ArchiveTo observe the clinical efficacy and safety of preoperative medication with lidocaine hydrochloride injection ultrasonic atomization combined with low-dose dexmedetomidine hydrochloride injection for fiberoptic bronchoscopy under general anesthesia in patients with pulmonary tuberculosis.
Patients with pulmonary tuberculosis scheduled for general anesthesia fiberoptic bronchoscopy were randomly divided into treatment group and control group. Both groups were given intravenous infusions of fentanyl citrate injection 0.05 mg and 1.5 mg·kg-1 propofol medium and long chain fat emulsion injection for induction of anesthesia. During the procedure, 2-3 mg·kg-1·h-1 propofol medium and long chain fat emulsion injection was used to maintain anesthesia. Control group received no additional treatment, while treatment group received an additional intravenous infusion of 0.2 μg·kg-1 dexmedetomidine hydrochloride injection through micro-pump over 15 min, combined with nebulized inhalation of lidocaine hydrochloride injection 3-4 mL, before induction of anesthesia. The postoperative anesthesia status, recovery quality, inflammation-related indicators and safety were compared between the two groups.
Among the 95 patients with pulmonary tuberculosis who underwent fiberoptic bronchoscopy under general anesthesia, 3 cases dropped out during the treatment and finally 46 cases were included in each group. After treatment, the loss of consciousness time in control group and treatment group were (172.65±36.81) and (146.67±26.46)s, respectively; the recovery time were (18.67±1.06) and (15.50±0.75) min, respectively; the orientation recovery time were (16.63±1.76) and (9.57±1.70) min and the dosage of propofol were (130.21±13.41) and (124.02±15.43) mg, respectively; the Ramsay scores of 10 minutes after awakening were (3.09±0.51) and (2.57±0.62) points, respectively; the Ramsay scores of 20 minutes after awakening were (3.52±0.55) and (3.00±0.67) points, respectively; the levels of death-associated protein kinase 1 (DAPK1) were (88.08±9.85) and (81.88±11.55) ng·L-1, respectively; the levels of NOD-like receptor family pyrin domain-containing 3 (NLRP3) were (78.63±9.35) and (73.96±7.52) ng·L-1, respectively; the levels of interleukin-1β (IL-1β) were (46.02±4.59) and (41.04±6.62) ng·L-1, respectively and the levels of IL-18 were (5.71±1.64) and (4.78±1.23) ng·L-1, respectively. The differences of the above indexes between treatment group and control group were statistically significant (all P<0.05). The main adverse drug reactions of control group were tinnitus, dizziness, nausea, agitation and convulsion; in treatment group were dizziness, nausea, agitation and convulsion, the total incidence of adverse drug reactions in control group was 13.04% (6 cases/46 cases), while that in treatment group was 8.70% (4 cases/46 cases). There was no statistically significant difference between the two groups (P>0.05).
Lidocaine hydrochloride injection combined with low-dose dexmedetomidine hydrochloride injection has significant advantages in patients with pulmonary tuberculosis undergoing fiberoptic bronchoscopy under general anesthesia. It can effectively improve the anesthetic effect and recovery quality of patients, reduce the dosage of propofol and reduce the levels of inflammatory factors with with good safety.
To study the efficacy and safety of allisartan isoproxil tablet combined with indapamide tablet in the treatment of patients with mild to moderate essential hypertension and coronary heart disease.
Patients with mild to moderate essential hypertension and coronary heart disease were divided into treatment group and control group using the cohort method. The control group was given oral indapamide tablets 2.5 mg once a day based on the conventional treatment regimen. The treatment group was given allisartan isoproxil tablets 240 mg once a day in addition to the control group’s regimen for a total of 12 weeks. The clinical efficacy, 24-hour blood pressure variability, cardiac function, vascular endothelial function and safety evaluation of the two groups were compared.
A total of 105 patients were enrolled, including 54 patients in treatment group and 51 patients in control group. After treatment, the total clinical effective rate of the treatment group was 90.74% (49 cases/54 cases), and that of control group was 72.55% (37 cases/51 cases), which was significantly higher in treatment group than in control group (P<0.05). After treatment, the daytime (d) systolic blood pressure variability (SBPV) levels in treatment group and control group were (11.32±2.13) and (12.48±2.26) mmHg, respectively; the nighttime (n) SBPV levels were (10.03±1.79) and (10.82±2.10) mmHg, respectively; the d diastolic blood pressure variability (DBPV) levels were (8.66±1.51) and (9.36±1.57) mmHg, respectively; the nDBPV levels were (8.05±1.32) and (8.68±1.62) mmHg, respectively; the 24 h SBPV levels were (10.85±2.20) and (11.96±2.05) mmHg, respectively; the 24 h DBPV levels were (9.67±1.93) and (10.66±1.92) mmHg, respectively; the brain natriuretic peptide (BNP) levels were (83.47±10.53) and (89.41±13.19) ng·L-1, respectively; the endothelin-1 (ET-1) levels were (55.44±9.27) and (60.36±10.86) ng·L-1, respectively; and the Apelin levels were (36.44±6.41) and (34.22±4.37) ng·mL-1, respectively. The above metrics showed significant differences between the two groups (P<0.05，P<0.01). The adverse drug reactions in treatment group included diarrhea, fever, fatigue, palpitations, soreness in both knee joints, cough, insomnia, decreased appetite and orthostatic hypotension. The adverse drug reactions in control group included diarrhea, headache, decreased appetite, insomnia and orthostatic hypotension. The total incidence of adverse drug reactions in treatment group was 22.22% (12 cases /54 cases), and that in control group was 17.65% (9 cases /51 cases). There was no statistically significant difference (P>0.05).
The application of allisartan isoproxil combined with indapamide in treatment of patients with mild to moderate essential hypertension and coronary heart disease can achieve significant therapeutic effects, regulate 24-hour blood pressure variability, improve cardiac function, vascular endothelial function, and quality of life, also demonstrate good safety.
To observe the clinical efficacy and safety of finerenone tablets combined with dapagliflozin tablets in the treatment of elderly diabetic nephropathy (DN).
Elderly patients with DN in hospital were divided into treatment group and control group. The patients in control group were treated with oral dapagliflozin tablets once a day in the morning, with a dose of 5 mg each time, while the patients in the treatment group were combined with finerenone tablets on the basis of control group, and adjusted according to the estimated glomerular filtration rate (eGFR) levels of patients. Serum creatinine (SCr), blood urea nitrogen (BUN), 24 h urine protein quantification, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), high-sensitivity C-reactive protein (hs-cRP), total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C) and clinical efficacy were compared between groups of patients, and the safety was evaluated.
A total 90 patients were enrolced; 45 in treatment group and 45 in control group. After treatment, the SCr levels in treatment group and control group were (127.63±10.28) and (140.27±11.95) μmol·L-1, BUN levels were (11.45±3.57) and (18.62±3.29) mmol·L-1, 24 h urine protein quantification levels were (99.28±11.42) and (117.92±12.00) mg·24 h-1, IL-6 levels were (12.32±2.15) and (16.41±3.50) ng·L-1, TNF-α levels were (31.68±10.52) and (43.09±11.83) ng·L-1, hs-cRP levels were (6.08±1.20) and (9.56±1.57) ng·L-1, TC levels were (4.49±0.55) and (4.83±0.72) mmol·L-1, TG levels were (2.57±0.63) and (2.79±0.48) mmol·L-1, LDL-C levels were (2.71±0.63) and (3.06±0.45) mmol·L-1 respectively, and the above indicators in treatment group were significantly lower than those in control group, with statistically significant differences (all P<0.05). The total clinical effective rate in treatment group was 93.34% (42 cases/45 cases), and that in control group was 75.56% (34 cases/45 cases), with statistically significant difference (P<0.05). The adverse drug reactions in treatment group were hypotension, hypoglycemia, acute kidney injury, hyperkalemia and pruritus, and the adverse drug reactions in control group included hypoglycemia, acute kidney injury and hyperkalemia. The total incidence rates of adverse drug reactions in treatment group and control group were 22.22% (10 cases/45 cases) and 8.89% (4 cases /45 cases) respectively, without statistically significant difference (P>0.05).
Compared with dapagliflozin tablets, the combined use of finerenone tablets for elderly DN can better improve the renal function, and regulate the lipid metabolism, with good safety.
To analyze the effect of urapidil sustained release capsules combined with finasteride tablet in the treatment of benign prostatic hyperplasia with lower urinary tract symptoms.
Patients with benign prostatic hyperplasia accompanied by lower urinary tract symptoms were included and randomly divided into treatment group and control group. Both groups received basic treatment with finasteride tablets, 5 mg each time, once daily, orally. The treatment group was treated with urapidil sustained release capsules, with an initial dose of 30 mg per day. If the patient’s clinical symptoms did not improve within 1-2 weeks, the dose could be gradually increased to 60 mg per day, with a maximum dose not exceeding 60 mg per day, twice a day, orally. Control group did not receive additional treatment. Compare the improvement of symptoms, quality of life, urodynamic indicators, laboratory indicators, clinical efficacy and evaluate safety between two groups.
A total of 45 patients in treatment group and control group were included respectively. Ten patients withdrew from the study due to lost to follow-up or personal factors during the study, 5 patients in each groups. Finally, a total of 80 patients completed the study, 40 patients in treatment group and 40 patients in control group. The total effective rate of treatment group was 95.00% (38 cases/40 cases), while that of control group was 80.00% (32 cases/40 cases), which was statistically significantly higher in treatment group than in control group (P<0.05). After treatment, the international prostate symptom score (IPSS) of treatment group and control group were (10.52±0.98) and (13.79±1.05) points; the prostate quality of life score (QoL) were (2.01±0.77) and (2.51±0.52) points, above indicators in treatment group were statistically significantly lower than those in control group (all P<0.05). After treatment, post-void residual urine volume (PVR) levels of treatment group and control group were (31.60±3.75) and (35.79±3.24) mL, respectively; the average urinary flow rates (AER) were (16.88±1.46) and (14.37±1.22) mL·s-1, respectively; the maximum urinary flow rates (Qmax) were (24.09±2.03) and (21.96±2.77) mL·s-1, respectively. The PVR level in treatment group was statistically significantly lower than that in control group, while the AER and Qmax levels were statistically significantly higher than those in the control group (all P<0.05). After treatment, the prostate-specific antigen (PSA) levels in treatment group and control group were (0.51±0.09) and (0.74±0.10) ng·L-1, respectively; the numbers of red blood cells in urine sediment were (37.41±3.06) and (40.25±3.22) cells per HP, respectively, and the above indicators in treatment group were statistically significantly lower than those in control group (all P<0.05). After treatment，the testosterone (T) levels in treatment group and control group were (974.05±16.87) and (929.78±16.77) ng·mL-1, respectively; the estradiol (E2) levels were (136.47±10.55) and (127.58±10.35) pg·mL-1, respectively. The above indicators in treatment group were significantly higher than those in control group (all P<0.05). The main adverse drug reactions in both groups were gastrointestinal discomfort, headache, etc. The incidence of adverse drug reactions in treatment group was 12.50% (5 cases/40 cases), while in control group was 5.00% (2 cases/40 cases). There was no statistically significant difference between the two groups (P>0.05).
Patients with benign prostatic hyperplasia accompanied by lower urinary tract symptoms were treated with combination therapy of urapidil sustained-release capsules and finasteride tablet, which improved their urodynamic indicators and clinical symptoms, restored their sex hormone levels, improved their treatment efficacy and quality of life.
To explore the clinical efficacy of fusidic acid ointment in patients with acne vulgaris who underwent non-ablative fractional 1 565 nm laser treatment.
Patients with common acne who received non-peeling fractional 1 565 nm laser treatment were divided into treatment group and control group. Treatment group was treated with fusidic acid ointment, 3 times a day, while control group was not treated with additional treatment.The lesion severity, skin sebum secretion, skin stratum corneum water content, clinical efficacy, matrix metalloproteinase 1 (MMP-1), matrix metalloproteinase tissue inhibitor-1 (TIMP-1), MMP-1/TIMP-1 ratio, skin elasticity indicators (R2, R5, R7), facial acne comprehensive grading system (global acne grading system, GAGS) score and acne-specific quality of life questionnaire (Acne-QOL) score were compared between the two groups.
100 patients with acne vulgaris who received non exfoliative dot matrix 1 565 nm laser were enrolled, including 50 cases in treatment group and 50 cases in control group. After treatment, the total clinical effective rate of treatment group was 96.00% (48 cases/50 cases), and that of control group was 74.00% (37 cases/50 cases), the difference was statistically significant (P<0.05). After 3 months treatment, the skin oil secretion of treatment group and control group were (53.79±7.23) and (69.21±10.67) μg·cm-2, respectively; the moisture content of cuticle were (34.21±5.15)% and (29.68±3.92)%, respectively; MMP-1 were (1.02±0.28) and (1.24±0.43) μg·mL-1, respectively; TIMP-1 were (1.62±0.24) and (1.43±0.20) μg·mL-1, respectively; MMP-1/TIMP-1 were 0.63±0.10 and 0.87±0.15, respectively; the R2 were (53.77±8.75)% and (49.11±7.64)%, respectively; the R5 were (53.88±8.58)% and (49.67±7.69)%, respectively; the R7 were (32.55±6.05)% and (28.39±5.44)%, respectively; the GAGS scores were (13.78±2.69) and (17.83±3.35) points, respectively; the Acne-QOL scores were (105.56±5.58) and (90.21±6.32) points, respectively. After treatment, the above indexes in treatment group were significantly lower than those in control group (all P<0.05). The adverse drug reactions in treatment group and control group were dry, tingling, scaling and flushing. The total incidence of adverse drug reactions in treatment group was 10.00% (5 cases/50 cases) and in control group was 16.00% (8 cases/50 cases). There was no significant difference in the incidence of adverse drug reactions between the two groups (P>0.05).
Fusidic acid ointment could significantly improve the dynamic balance of MMP-1/TIMP-1, skin elasticity and skin physiological indexes in patients with acne vulgaris receiving non-ablative fractional 1 565 nm laser, with good safety.
To investigate the influence of augmented renal clearance (ARC) on the steady-state serum concentration and pharmacodynamics of meropenem in patients with severe infections and to analyze the linear relationship between them.
A retrospective analysis was conducted on the inpatients who received meropenem treatment and underwent therapeutic drug monitoring (TDM) at the Fifth Medical Center of the General Hospital of the PLA from June 2021 to September 2024. Serum drug concentration data were collected, and pharmacokinetic parameters were calculated using a one-compartment model. The steady-state serum concentrations and pharmacodynamic parameters were compared between patients with normal renal function and those with ARC. Multiple linear regression analysis was performed to explore the factors influencing meropenem serum concentrations and pharmacodynamic parameters.
When meropenem was administered at a dose of 1.0 g three times daily, the blood concentrations in patients with ARC at 3 hours and 0.5 hours before the last administration were (4.78±2.34) mg·L-1 and (2.44±1.60) mg·L-1, respectively. In contrast, the corresponding concentrations in patients with normal renal function were (14.08±10.45) mg·L-1 and (8.40±7.07) mg·L-1, respectively. The blood concentrations of meropenem were significantly lower in ARC patients compared to those with normal renal function (P<0.05). For the pharmacodynamic target of f%T>4MIC≥40%, the target attainment rates in ARC patients were 81.25%, 25.00%, 0.00%, and 0.00% at MIC values of 1, 2, 4, and 8 μg·mL-1, respectively. In comparison, the rates in patients with normal renal function were 92.31%, 76.92%, 53.85%, and 7.69%, respectively, indicating significantly lower target attainment in the ARC group. Multiple linear regression analysis revealed that creatinine clearance rate and serum albumin level significantly influenced both the plasma concentration and pharmacodynamic target attainment of meropenem.
ARC significantly reduces the steady-state serum concentration of meropenem and the rate of achieving pharmacodynamic targets, leading to the failure of anti-infective therapy. For patients with severe infections and ARC, attention should be paid to the effects of creatinine clearance, serum albumin on serum drug concentrations and therapeutic efficacy. TDM should be performed to adjust the dosing regimen in a timely manner.
To investigate the effects of daptomycin (DAP) on the proliferation, apoptosis, and cell cycle of U266 [U266B1] human multiple myeloma cells (U266).
U266 cells were divided into the following groups: normal control group (NC group), DAP 20 μM group (DAP20), DAP 40 μM group (DAP40), DAP 80 μM group (DAP80), BZ 50 nM group (BZ50), and DAP 80 μM + BZ 50 nM group (DAP80+BZ50). U266 cells were treated with varying concentrations of DAP (0, 20, 40, and 80 μM), 50 nM bortezomib (BZ), and combination of DAP (80 μM) plus BZ (50 nM). Effects were assessed using cell counting kit-8 (CCK-8) assays, Western blotting (WB), flow cytometry, and quantitative real-time polymerase chain reaction (qPCR).
At 24 h post-treatment: Cell viability rates were recorded as (97.13±2.51)%, (96.80±3.44)%, (85.48±3.28)%, (81.56±2.09)%, (60.78±2.80)%, and (38.09±2.09)% for DAP alone (0-80 μM), BZ monotherapy, and combinatorial treatment, respectively. Early apoptotic cell proportions measured via flow cytometry showed values of (7.50±0.84)%, (8.20±1.41)%, (9.07±1.22)%, (13.14±2.27)%, (14.51±2.58)%, and (15.17±1.87)% across groups. Proportions of cells in G1 phase were determined to be (33.40±1.48)%, (33.03±2.49)%, (31.50±1.40)%, (38.59±1.54)%, (36.94±1.13)%, and (39.43±1.40)%. Relative expression levels of ribosomal protein S19 (RPS19) mRNA exhibited fold changes of 0.99±0.09, 1.00±0.14, 0.66±0.04, 0.61±0.06, 0.55±0.04, and 0.53±0.07, while corresponding protein levels via WB analysis were 1.08±0.05, 0.97±0.03, 0.90±0.02, 0.87±0.04, 0.89±0.04, and 0.57±0.03. Statistically significant differences (all P<0.001) were observed in BZ50, DAP80, and their combination compared to DAP 0 μM group.
DAP may exert its inhibitory effect on U266 cell proliferation and promote apoptosis by downregulating the expression of RPS19. This study provides a potential therapeutic drug for the treatment of multiple myeloma.
To investigate the effect of emodin (Emo) on chemotherapy resistance of human leukemia K562/adriamycin-resistant (K562/ADR) cells and its mechanism.
K562/ADR cells were assigned to control group and experimental -L, -M, -H groups. Experimental -L, -M, -H groups were incubated with Emo at concentrations of 5, 10, and 20 μmol·L-1, respectively. Control group was treated with 0.1% dimethyl sulfoxide. Methyl thiazolyl tetrazolium (MTT) assay was used to detect the effect of Emo on chemotherapy resistance in K562/ADR cells. Fluorescence analysis was used to detect the intracellular accumulation of adriamycin. Flow cytometry was used to detect the cell cycle and apoptosis. Polymerase chain reaction was used to detect the mRNA expression level of P-glycoprotein (P-gp). In addition, Western blot was used to detect the protein expression level of P-gp and nuclear factor-kappa B (NF-κB) pathway related proteins.
The half maximal inhibitory concentrations (IC50) of K562/ADR cells to adriamycin in experimental -M, -H groups and control group were (20.91±2.03), (11.79±0.89) and (38.00±2.61) μg·ml-1; the intracellular adriamycin-associated mean fluorescence intensities (×104) were (5.22±0.66), (7.47±0.77) and (2.69±0.69); the proportions of G0/G1 phase cells were (37.81±3.47)%, (28.05±2.86)% and (51.18±5.06)%; the proportions of S phase cells were (19.89±2.98)%, (15.24±2.21)% and (32.15±3.20)%; the proportions of G2/M phase cells were (40.65±3.33)%, (55.75±4.55)% and (13.63±2.29)%; the cell apoptosis rates at 48 hours were (39.91±3.51)%, (46.26±4.06)% and (21.45±1.92)%; the relative expression levels of P-gp mRNA were 68.10±9.61, 31.01±8.90 and 100.00±12.22; the relative expression levels of P-gp protein were 77.01±8.31, 63.65±7.72 and 100.00±7.07; the relative expression levels of p65 (RelA/p65) in nucleus were 126.10±8.17, 157.58±11.87 and 100.00±8.55; the relative expression levels of phosphorylated-inhibitor of nuclear factor κB protein α (p-IκBα) in cytoplasm were 132.45±13.46, 150.97±9.47 and 100.00±7.35; the relative expression levels of IκBα in cytoplasm were 82.10±5.95, 73.20±6.39 and 100.00±5.84; the relative expression levels of phosphorylated-inhibitor of kappa B kinase α/β (p-IKKα/β) in cytoplasm were 126.23±6.63, 120.61±7.70 and 100.00±7.96, respectively. Compared the above indexes of the experimental -M and experimental -H groups with those of the control group, and the differences were statistically significant (P<0.05, P<0.01, P<0.001).
Emo can inhibit adriamycin chemotherapy resistance in K562/ADR cells by activating the NF-κB pathway and subsequently down-regulating the expression of P-gp.
To explore the potential of anti-programmed cell death ligand 1 (PD-L1) immunotherapy in giant congenital melanocytic nevus (GCMN) treatment.
GCMN cells were divided into four groups: GCMN group (GCMN cells alone), unactivated peripheral blood mononuclear cells (PBMC)+GCMN group (GCMN cells with unstimulated PBMCs), activated PBMC+GCMN group (GCMN cells with CD3/CD28 antibody-stimulated PBMCs), and activated PBMC+GCMN+PD-L1 inhibitor group (the activated PBMC +GCMN group treated with 10 μg·mL-1 PD-L1 inhibitor atezolizumab). After 72 hours of culture, cell cytotoxicity and confluence were assessed. Cell viability was measured using the cell counting kit (CCK-8) assay, and apoptosis was evaluated via flow cytometry. Additionally, a humanized immune system was established in C-NKG severely immunodeficient mice by intraperitoneal injection of human PBMCs. A GCMN patient-derived xenograft (PDX) model was constructed in these humanized mice, divided into two groups: control group [phosphate buffer saline (PBS)] and experimental group (intraperitoneal injection of 10 mg·kg-1 atezolizumab), administered every 3 days for 2 weeks, to evaluate in vivo efficacy.
Cell confluence rates for the GCMN, unactivated PBMC+GCMN, activated PBMC+GCMN, and activated PBMC+GCMN+PD-L1 inhibitor groups were (93.14±3.25)%, (85.29±2.40)%, (68.29±3.68)% and (22.55±4.28)%, respectively. Cell viability rates were (100.00±1.48)%, (80.35±2.60)%, (52.17±2.37)% and (15.61±1.82)%, respectively. Apoptotic cell proportions were (0.64±0.14)%, (9.32±0.91)%, (19.29±3.98)% and (28.43±0.33)%, respectively. Compared to the GCMN group, the activated PBMC+GCMN+PD-L1 inhibitor group showed statistically significant differences in all measured parameters (all P<0.05). In GCMN-PDX model, dermal cell density in experimental group and control group were (580±183) and (3 658±532) cells·mm-2, respectively. And the difference of the above index between the two groups was statistically significant (all P<0.05).
This study demonstrates that PD-L1 inhibitors effectively target GCMN cells by activating the immune system, offering a promising new strategy for the clinical treatment of GCMN.
To investigate the improving effect of ginseng (GS) on metoprolol（meto） induced bradycardia in mice with chronic heart failure（CHF）and its molecular mechanism.
The CHF model in C57BL/6J mouse was established through left anterior descending coronary artery ligation. Mice were randomly divided into 6 groups, including sham group（underwent the same surgical procedure without coronary artery ligation）, model group, control group（26 mg·kg-1·d-1 metoprolol）, experimental-low group（26 mg·kg-1·d-1 metoprolol + 1.3 g·kg-1·d-1 GS）, experimental-midium group（26 mg·kg-1·d-1 metoprolol + 2.6 g·kg-1·d-1 GS）and experimental-high group（26 mg·kg-1·d-1 metoprolol + 5.2 g·kg-1·d-1 GS）. Each group contained 9 mice. After continuous administration for 8 weeks, heart rate changes were monitored using non-invasive blood pressure monitors in small animals; transcriptome sequencing was employed to analyze differentially expressed genes in cardiac tissues with functional enrichment analysis; calcium ion concentration in myocardial tissue was measured using a calorimetric assay; Western blot analysis was used to detect relative expression levels of sarcoplasmic reticulum calcium ATPase 2a（SERCA2a）, phosphorylated phospholamban（p-PLB）and sodium-calcium exchanger 1（NCX1）in myocardial tissue.
The heart rates of sham group, model group, control group and experimental-L, -M, -H groups were（528.61±60.86），（448.67±84.58）,（260.07±74.97）,（352.84±40.47）,（436.27±90.84）and（501.91±43.11）beats·min-1, respectively. Control group was compared with model group, experimental-L, -M, -H groups were compared with control group, the differences showed statistical significance in heart rates（P<0.05，P<0.01）. Transcriptome gene ontology（GO）analysis revealed that differentially expressed genes were significantly enriched in pathways related to myocardial contraction and calcium ion transmembrane transport（all P<0.05）. The myocardial tissue calcium ion concentrations in sham group, model group, control group and experimental-L, -M, -H groups were（30.09±2.36）,（35.97±1.15）,（16.15±2.37）,（19.59±1.04）, （23.64±0.54）and（28.54±2.82）mmol·L-1，respectively. Compared with control group, experimental-L, -M, -H groups all showed significantly increase（P<0.01, P<0.05）. The relative expression levels of SERCA2a in sham group, model group, control group and experimental-L, -M, -H groups were 1.00±0.14, 0.83±0.05, 1.23±0.12, 1.00±0.03, 0.98±0.05 and 0.90±0.11, respectively; the relative expression levels of p-PLB were 1.38±0.24, 1.05±0.19, 2.12±0.35, 1.08±0.24, 0.54±0.57,and 0.52±0.13; while the relative expression levels of NCX1 were 1.00±0.13, 1.08±0.20, 1.69±0.34, 1.06±0.35, 1.15±0.22 and 0.81±0.21. Compared with model group, the relative expression levels of all 3 proteins in control group showed significant increases. Except for SERCA2a in experimental -L group and NCX1 in experimental -M group, the relative expression levels of the above three proteins in the experimental group were significantly lower than that in the control group (P<0.01, P<0.05).
Meto may induce bradycardia adverse drug reaction by increasing the p-PLB/PLB ratio and elevating the expression levels of SERCA2a and NCX1 proteins, which reduces intracellular free calcium ion concentration in cardiomyocytes. Ginseng could significantly down regulate the p-PLB/PLB ratio, increase the protein expression levels of SERCA2a and NCX1, and up regulate the concentration of intracellular free calcium ion, so as to improve Meto induced bradycardia, suggesting that it may antagonize the negative frequency effect of Meto by remodeling the calcium cycle homeostasis.
To investigate the effects of gastrodin (GAS) on diabetes-induced cardiomyopathy (DCM) and its underlying mechanisms.
Fifty C57BL/6J mice were divided into control group (n=10, normal diet) and high-fat high-sucrose (HFD) group [n=40, HFD diet combined with intraperitoneal streptozotocin (STZ) injection to establish the DCM model]. Successfully modeled HFD mice were randomly assigned to the model group, GAS low-dose group (50 mg·kg-1, qd), GAS high-dose group (100 mg·kg-1 qd), and positive control metformin group (250 mg·kg-1，qd). The control and model groups were administered saline via gavage, while the other three groups received their respective drugs via gavage for three consecutive months. Cardiac ultrasound was used to measure left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular end-systolic volume (LVESV), and left ventricular internal diameter at end-systole (LVIDs). Serum levels of triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) were quantified using assay kits. Cardiac tissue levels of malondialdehyde (MDA) and glutathione (GSH) were measured. Protein expression was analyzed via Western blotting.
The LVEF of the model group and high-dose group were (62.54±3.24)% and (80.20±3.29)%, respectively, and the LVFS were (25.87±4.75)% and (42.97±4.75)%, respectively LVESVs were (55.00±4.08) and (23.75±4.79) μL, LVIDs were (2.63±0.16) and (1.67±0.21) mm, TG was (1.17±0.18) and (0.51±0.09) mmol·L-1, TC was (5.58±0.76) and (1.93±0.58) mmol·L-1, HDL-C was (1.69±0.50) and (4.86±0.48) mmol·L-1, LDL-C was (3.84±0.70) and (1.17±0.65) mmol·L-1, respectively. The MDA content was (6.10±0.38) and (3.02±0.16) nmol· mgprot-1, the GSH content was (20.90±10.30) and (39.49±15.70) μmol·gprot-1, the relative expression levels of oxidative stress protein Kelch like ECH associated protein 1 (Keap1) were 1.75±0.22 and 1.07±0.03, the relative expression levels of nuclear factor-E2-related factor 2 (Nrf2) were 0.51±0.09 and 0.96±0.13, and the relative expression levels of peroxidase-1 (PRDX-1) were 0.43±0.08 and 0.93±0.18, respectively, and the relative expression levels of heme oxygenase-1 (HO-1) were 0.42±0.08 and 0.94±0.14, respectively. Compared with the model group, the above indicators in the high-dose group showed statistically significant differences (P<0.01，P<001).
GAS can improve the myocardial function of DCM mice, and its mechanism of action may be related to the inhibition of oxidative stress and the regulation of the Keap1/Nrf2 signaling pathway.
To investigate the protective effect and mechanism of astragaloside Ⅳ (AS-Ⅳ) on intestinal injury and secondary liver injury in rats with ulcerative colitis (UC) induced by trinitrobenzene sulfonic acid (TNBS).
Wistar rats were randomly divided into normal control group, UC model group and AS-Ⅳ experimental low, medium and high dose groups, with 10 rats in each group. The UC rat model was prepared by TNBS enema. AS-Ⅳ (25, 50, 100 mg·kg-1) or sulfasalazine (SASP, 300 mg·kg-1) was administered intragastrically for 6 consecutive days starting from the second day after modeling. The general condition, colonic histopathological score, and liver function of the rats were examined. The levels of inflammatory factors in serum, colon and liver tissues were detected by enzyme-linked immunosorbent assay (ELISA). The expressions of tight junction proteins (ZO-1, Occludin) in colon and antioxidant enzymes in liver tissues were detected by Western blot.
In the normal group, model group, low, medium and high dose experimental groups, the serum TNF-α levels were (246.30±23.39), (308.70±61.39), (279.10±45.76), (240.80±16.61) and (233.60±30.14) pg·mL-1, and the serum IL-1β levels were (23.93±14.82), (82.42±20.84), (69.46±22.23), (40.92±11.21) and (35.42±10.34) pg·mL-1，respectively. The intestinal TNF-α levels were (101.60±11.18), (158.70±23.47), (146.40±17.90), (115.70±21.06) and (91.84±21.57) pg·mL-1, and the intestinal IL-1β levels were (724.60±78.73), (1 043.00±106.32), (836.35±103.35), (774.60±133.68) and (694.50±40.84) pg·mL-1，respectively. The relative expression levels of tight junction protein ZO-1 in colon tissue were 1.01±0.01, 0.48±0.01, 0.46±0.01, 0.61±0.09 and 1.15±0.10, and the relative expression levels of tight junction protein Occludin in colon tissue were 1.00±0.01, 0.64±0.11, 0.57±0.13, 0.73±0.10 and 1.02±0.13，respectively. The levels of TNF-α in liver tissues were (1 727.00±223.70), (2 008.00±220.40), (1 762.00±45.19), (1 723.00±49.45), and (1 680.00±103.10) pg·mg-1, and the levels of IL-1β in liver tissues were (1 317.00±331.40), (2 158.00±730.90), (1 546.00±258.90), (1 806.00±523.40), and (1 121.00±84.62) pg·mg-1. The MDA levels in liver tissues were (0.98±0.15), (1.51±0.29), (1.29±0.30), (1.15±0.12) and (1.06±0.21) nmol·mg-1, the reduced glutathione (GSH) levels in liver tissues were (8.46±0.60), (5.84±0.49), (6.30±0.27), (7.48±0.50) and (8.07±0.60) μmol·gProt-1, the glutathione peroxidase (GSH-PX) levels in liver tissues were (666.90±68.39), (481.00±19.16), (562.80±45.61), (620.20±12.13) and (658.80±18.11) U·mgProt-1.The above indicators in the medium and high dose experimental groups were statistically significant compared with the model group (all P<0.05).
AS-IV can effectively improve intestinal and liver injury in rats with UC induced by TNBS. The mechanism may be related to repairing intestinal mucosal barrier, inhibiting inflammatory response and improving liver antioxidant function.
To explore the roles of oxidative stress and apoptosis in the renal deficiency and blood stasis type oligoasthenozoospermia（OAS） model, and to investigate the mechanism of the intervention by the Qi-supplementing, Blood-activating and Essence-nourishing formula.
The rat model of renal deficiency and blood stasis type oligoasthenozoospermia was established by intragastric administration of Gentiana macrophylla polysaccharides (GTW). The rats were randomly divided into the model group, the levocarnitine group, the low, medium and high doses of the Qi-supplementing, Blood-activating and Essence-nourishing formula groups; another 8 rats were randomly selected as the normal control group. The levocarnitine group was intragastrically administered 1.8 mL·kg-1 levocarnitine oral liquid; the low, medium and high doses of the Qi-supplementing, Blood-activating and Essence-nourishing formula groups were given 7.87, 15.75 and 31.50 g·kg-1，respectively; the blank group and the model group were intragastrically administered the same amount of 0.9% NaCl. All 6 groups of rats were administered the drugs once daily and continuously for 28 days. The general conditions of the rats were observed; the testicular and epididymal indices were measured; the sperm quality was detected; the pathological morphology of the testicular tissue was observed by hematoxylin-eosin staining (HE); the activity of reactive oxygen species (ROS), catalase (CAT) and superoxide dismutase (SOD) in the testicular tissue was detected by enzyme-linked immunosorbent assay (ELISA); the mRNA expression levels of Caspase-3, Bcl-2 and Bax in the testicular tissue were detected by real-time fluorescence quantitative polymerase chain reaction (q-PCR).
The testicular indices of the blank group, model group, low, medium and high doses of the Qi-supplementing, Blood-activating and Essence-nourishing formula group, and the levocarnitine group were (0.83±0.09)%, (0.55±0.10)%, (0.55±0.07)%,(0.71±0.12)%,(0.81±0.08)%, and (0.67±0.07)%, respectively; the epididymal indices were (0.36±0.05)%, (0.24±0.03)%, (0.25±0.04)%, (0.28±0.02)%,(0.35±0.06)%, and (0.28±0.03)%,respectively; the sperm concentrations were (24.11±11.64, 4.65±2.48, 6.75±3.81, 11.60±7.78, 21.72±7.81, 23.22±8.80)×106 sperm·mL-1, respectively; the sperm motility was (86.93±12.00)%, (33.46±16.13)%, (53.01±21.71)%, (63.15±24.35)%, (79.97±10.22)%, and (75.83±25.05)%, respectively; the ROS intensity was 597 926.11±87 518.20, 925 239.02±95 539.79, 846 676.84±64 867.76, 784 277.73±81 354.32, 658 228.04±82 768.68, and 725 740.12±87 846.36, respectively; the CAT activity was (1.40±0.11), (0.56±0.09), (0.77±0.11), (0.95±0.13), (1.15±0.12), and (1.03±0.11) U·mgprot-1, respectively; the SOD activity was (2.41±0.07), (1.65±0.05), (1.79±0.33), (1.90±0.04), and (2.21±0.05), and (2.06±0.04) U·mgprot-1, respectively. the relative expression levels of Bcl-2 mRNA were 1.00±0.04, 0.26±0.02, 0.39±0.04, 0.49±0.02, 0.87±0.02, and 0.66±0.05, respectively; the relative expression levels of Bax mRNA were 1.00±0.05, 1.78±0.07, 1.50±0.04, 1.39±0.02, 1.12±0.04, and 1.27±0.04, respectively; the relative expression levels of Caspase-3 mRNA were 1.00±0.03, 1.95±0.06, 1.81±0.03, 1.68±0.03, 1.18±0.07, and 1.49±0.08, respectively. The above-mentioned indicators of the model group compared with the blank group, the high-dose group compared with the model group, and the L-carnitine group except for the epididymal index compared with the model group, all showed statistically significant differences (P<0.05，P<0.01).
Oxidative stress and cell apoptosis play multiple regulatory roles in the sperm quality and testicular damage of OAS rats. The Qi-supplementing, activating blood, and tonifying essence formula may improve the sperm quality and testicular function of rats by inhibiting oxidative stress and cell apoptosis.
To evaluate the bioequivalence of the test preparation and the reference preparation in a single dose of vortioxetine hydrobromide tablets under fasting and fed conditions in healthy volunteers.
A randomized, open-ended, single-dose, two-cycle, double-cross bioequivalence trial design was adopted, and 28 subjects were enrolled in the fasting group and the fed group, respectively, and 1 tablet of the test preparation and the reference preparation were taken in the fasting or fed state each cycle. The concentration of vortioxetine in plasma was determined by liquid chromatography-tandem mass spectrometry （LC-MS/MS） method. The main pharmacokinetic parameters were calculated by Phoenix WinNonlin 8.1, and the bioequivalence was evaluated.
The t1/2 for the fasting single oral administration of the test preparation and the reference preparation were （61.74±23.90） and （58.22±18.61）h, the median Tmax were （7.33±2.15） and （7.61±3.89） h, the Cmax were （7.32±1.90） and （7.46±1.98） ng·mL-1, and the AUC0-72 h were （312.61±92.95） and （310.00±93.84） h·ng·mL-1, respectively. The statistical results of the 90% confidence intervals of the main pharmacokinetic parameters Cmax and AUC0-72 h were 92.75%-103.71% and 97.47%-104.43%, respectively, all of which were within the range of 80.00%-125.00%, and the safety of the tested preparation and the reference preparation was good when taken orally on an empty stomach. The t1/2 of single oral administration after prandial administration of the tested preparation and the reference preparation were （77.60±33.87） and （81.61±45.24） h, the median Tmax were （8.06±3.02） and （7.77±2.45）h, the Cmax were （7.54±2.08） and （7.76±2.00） ng·mL-1, and the AUC0-72 h were （319.75±87.71） and （326.03±86.64） h·ng ·mL-1, respectively. The 90% confidence intervals of Cmax, AUC0-72 h were 89.00%-105.32% and 92.21%-102.72%, respectively, which were in the range of 80.00%-125.00%.
In the state of fasting and fed single oral administration, the two kinds of vortioxetine hydrobromide tablets have good bioequivalence.
To evaluate the bioequivalence and safety of colchicine tablets under fasting and fed conditions in Chinese healthy participants.
A single-center, randomized, open, single-dose, two-formulation, two-period, two-sequence crossover design was adopted, enrolling 72 healthy participants, with 36 healthy participants in each group for fasting and fed conditions. Single oral dose 0.5 mg of test formulation (T) or the reference formulation (R) was taken across two periods，respectively. Plasma concentration of colchicine was determined using ultra-high performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). The pharmacokinetic parameters were calculated and the bioequivalence was evaluated using the non-compartmental model in Phoenix WinNonlin 8.2 software.
The main pharmacokinetic parameters of a single oral colchicine tablet under fasting condition for T and R were as follows: Cmax were (2.70±0.88) and (2.54±0.87) ng·mL-1，tmax were 0.98 (0.48, 2.00) and 0.98 (0.73, 2.48) h，t1/2 were (29.54±5.46) and (29.67±4.86) h，AUC0-t were (18.40±5.30) and (18.00±5.10) h·ng·mL-1，AUC0-∞ were (21.80±5.90) and (20.70±4.90) h·ng·mL-1, respectively. The main pharmacokinetic parameters under fed condition for T and R were as follows: Cmax were (2.49±0.84) and (2.58±1.00) ng·mL-1，tmax were 1.48 (0.73, 3.98) and 1.48 (0.73, 4.00) h，t1/2 were (31.79±4.69) and (30.65±4.91) h，AUC0-t were (19.80±4.30) and (19.90±5.00) h·ng·mL-1，AUC0-∞ were (23.20±5.00) and (23.10±5.20) h·ng·mL-1, respectively. The geometric mean ratios of Cmax, AUC0-t and AUC0-∞ of the T and R formulations under fasting and fed conditions with a 90% confidence interval ranged from 80.00% to 125.00%.
Under both fasting and fed conditions, the colchicine tablet test formulation and reference formulation were bioequivalent in Chinese healthy subjects, and both were shown to be safe.
To establish and validate a highly sensitive and selective high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS) method for the determination of lurasidone, which was used subsequently to clinical lurasidone blood drug concentration monitoring.
Tadalafil was used as internal standard. Following a deproteinization procedure, lurasidone and the internal standard (tadalafil) were isostatically eluted using a mobile phase composed of methanol and 0.1% aqueous formic acid (50：50, v/v) at a flow rate of 0.70 mL·min-1. The chromatographic separation was achieved within 4.0 min on an Agilent ZORBAX Eclipse plus C8(4.6 mm×100.0 mm，3.5 μm). Quantification was performed using a triple-quadrupole mass spectrometer operating in positive electrospray ionization (ESI) mode with multiple reaction monitoring (MRM). The method was validated for selectivity, linearity (calibration curve), precision and accuracy, matrix effect, extraction recovesise, stability and dilutive integrity. The concentrations of 14 clinical samples were measured after this method was validated.
The calibration curve for lurasidone in human plasma demonstrated linearity over the concentration range of 0.50-500.00 ng·mL-1. The precision data (both intra- and inter-day) for the three QC levels ranged from 2.87% to 10.03%. Accuracy (relative error) was within±15% of the nominal values. The plasma samples maintained stability for 28 h at room temperature, for 85 days at -20 ℃ and through five freeze-thaw cycles. The measured concentrations of clinical samples were within the range of the standard curve, with concentrations ranging from 2.63 to 21.17 ng·mL-1.
The validated method is proved to be convenient, accurate, and sensitive for the quantification of lurasidone in human plasma. The method is proved to be suitable for the monitoring of plasma concentration and pharmacokinetics study of lurasidone.
A 76 years old female patient was hospitalized twice for pulmonary infection and bronchiectasis with infection. During her first admission to the respiratory department for pulmonary infection, she received intravenous cefoperazone sodium/sulbactam sodium combined with bronchodilators for 11 days and was discharged following clinical improvement, with no documented adverse drug reactions (ADRs). During her second presentation to the emergency department for bronchiectasis exacerbation, the patient developed cyanosis and profuse sweating 13 minutes after intravenous cefoperazone/sulbactam administration. Despite successful resuscitation and subsequent transfer to the intensive care unit (ICU), emergency physicians failed to recognize this event as a suspected drug hypersensitivity reaction or document it in the medical records. After 11 days of meropenem therapy and symptomatic management in the ICU, she was transferred back to the respiratory department. Respiratory physicians initiated antibiotic de-escalation by readministering cefoperazone/sulbactam, which precipitated respiratory distress, profuse sweating and systemic discomfort within 19 minutes, followed by loss of consciousness and cardiopulmonary arrest. The patient died after 48 hours of unsuccessful resuscitation. This case serves as a reminder that the sensitization period for drugs can persist from several days to several months. The absence of ADRs with previous use does not entirely preclude the risk of subsequent administration. The recognition of hypersensitivity is critical, necessitating enhanced vigilance among healthcare professionals regarding ADRs. The documentation of ADRs and handover procedures during transfers between departments should not be overlooked to ensure medication safety.
The newly revised The International Council for Harmonizsation of Technical Requirements for Pharmaceuticals for Human Use (ICH) E6 R(3) sets out internationally accepted principles and standards for conducting clinical trials. The application of innovative technologies in clinical trials, consideration of risk proportionality, and the development of new models are all important drivers for the revision of ICH E6 R(3). The main features of this revision include: alignment with “ICH E8 R(1) General Considerations for Clinical Studies,” restructuring of the document, provision of guidance on data governance, encouragement of risk-proportionate and fit-for-purpose approaches, and the establishment of practical and feasible expectations for sponsors and investigators. The revision also adapts to innovations in clinical trial design, technology, conduct, and data sources; strengthens the protection of minor trial participants; emphasizes transparency in clinical trial registration and results reporting; and updates terminology. The revision of ICH E6 R(3) impacts sponsors, investigators, ethics committees, and service providers, offering guidelines that are both practical and flexible, and continuously responding to the rapid development of the clinical trial ecosystem.
Bone-related infections represent a significant challenge in orthopedic practice, and the penetration efficacy of antimicrobials into bone tissue serves as a critical determinant of therapeutic outcomes. This review systematically summarizes the bone penetration characteristics of clinically used antimicrobial agents. Current evidence indicates that most β-lactam antibiotics demonstrate bone penetration rates ranging from 10% to 50%, while fluoroquinolones exhibit higher penetration at 30%-100%. Vancomycin and teicoplanin display penetration rates between 10% and 40%. Notably, clindamycin, linezolid and rifampicin achieve penetration rates exceeding 30%. Multiple factors influence drug penetration characteristics, including anatomical bone site variations, local blood perfusion status, patients’ pathophysiological conditions, as well as administration routes and dosage regimens.
Diabetic kidney disease (DKD) is a clinical syndrome in which diabetes leads to microvascular lesions and then glomerulosclerosis. In the progression of DKD, the hypoxia inducible factor-1α (HIF-1α) signaling pathway is involved in the occurrence, development and pathological formation of DKD. Related studies have shown that the HIF-1α pathway is the most critical pathway for the treatment of DKD with traditional Chinese medicine. Among them, Chinese medicine monomers, Chinese medicine compounds, and Chinese patent medicines play a role in preventing interstitial fibrosis and glomerulosclerosis by regulating the HIF-1α pathway. Its mechanism is closely related to inflammation, oxidative stress, cell apoptosis, and ferroptosis. This article reviews the existing research results on the treatment of DKD with the intervention of traditional Chinese medicine in the HIF-1α pathway in recent years, in order to provide a theoretical basis for the prevention and treatment of DKD and the development of new drugs.
The clinical isolation rate of carbapenem-resistant Acinetobacter baumannii (CRAB) has been increasing year by year, yet effective antimicrobial agents against this pathogen remain severely limited. Sulbactam-durlobactam, a novel β-lactam combination agent, has demonstrated promising in vitro antibacterial activity against CRAB. In May 2023, the U.S. Food and Drug Administration approved its use for patients aged 18 and older to treat hospital-acquired bacterial pneumonia and ventilator-associated bacterial pneumonia caused by susceptible isolates of the Acinetobacter baumannii-calcoaceticus complex, providing a new therapeutic option. This article reviews the mechanism of action, pharmacokinetics, pharmacodynamics, and clinical studies of sulbactam-durlobactam based on literature, aiming to offer insights for clinical practice.
Acute lung injury (ALI) is a severe respiratory disease. Given the limited existing treatment methods, it is urgent to explore new therapies. Pyroptosis plays a crucial role in the onset of ALI. Traditional Chinese medicine can regulate the pathways related to pyroptosis, reduce the inflammatory response, and improve acute lung injury, thus providing new strategies for the treatment of ALI. This article systematically reviews the mechanisms by which pyroptosis causes ALI in alveolar macrophages, neutrophils, and pulmonary vascular endothelial cells, summarizes the published literature from 2019 to 2024, and explores the action mechanisms of active ingredients and compound prescriptions of traditional Chinese medicine in the treatment of ALI, aiming to provide a theoretical basis for the research and development of new drugs.
Vancomycin is the first-line drug for treating infections caused by methicillin-resistant gram positive bacteria in patients with malignant hematological diseases. However, due to significant differences in the physiological and pathological characteristics of these patients compared to the general population, the pharmacokinetic behavior of vancomycin in the body may undergo significant changes. These changes may lead to unpredictable therapeutic effects, increased safety risks, and the evolution of bacterial resistance. Personalized dosing strategies may offer potential solutions to address these issues. Nevertheless, at present, there is a lack of unified, guideline-based, or consensus-driven reference standards for personalized dosing in these patients, particularly adult patients, and relevant research data remain insufficient. This review systematically summarizes the current status of pharmacokinetic studies on vancomycin in adult patients with malignant hematological diseases and focuses on the analysis of population pharmacokinetic models and their application progress. Additionally, this paper provides a detailed discussion of the current technical approaches available for vancomycin personalized dosing, including techniques based on therapeutic drug monitoring, clinical decision support systems, novel technical methods, and the latest dynamic dosing techniques developed by our research team based on individualized dosing models. Through an organized review of existing research, this paper identifies the challenges faced in achieving broader implementation of personalized dosing. It is hoped that this study will provide valuable insights for achieving personalized vancomycin dosing in patients with malignant hematological diseases, thereby advancing clinical practice and technological development in this field.
The treatment of posterior segment diseases has always been a challenge in the field of ophthalmology. How to overcome obstacles in drug delivery and improve the bioavailability of drugs in the posterior segment of the eye is one of the most challenging aspects in the field of drug research. The innovation of drug delivery routes and dosage forms, as well as breakthroughs in drug development, have brought new hope for the delivery of drugs in the posterior segment of the eye. This article reviews three aspects of innovative drug delivery routes for subretinal drug delivery, suprachoroidal drug delivery, and vitreous cavity implantation, innovative drug delivery form design for nano-formulations and exosomal formulations, and innovative drug development for intraocular injections, topical drops, and oral drugs, with the aim of providing new strategies for the treatment of diseases of the posterior segment of the eye.
Precancerous lesions of gastric cancer (PLGC) are considered as a high-risk factor for the development of gastric cancer. Existing studies have confirmed that hypoxia inducible factor-1α (HIF-1α) plays a key role in the progression of PLGC. HIF-1α promotes the malignant transformation of PLGC by regulating various cellular processes, including angiogenesis, aerobic glycolysis, autophagy, cell proliferation, and apoptosis. Traditional Chinese medicine (TCM) has been shown to modulate the HIF-1α signaling pathway and inhibit these pathological processes, thereby intervening in the development of PLGC. This review will focus on the mechanisms by which HIF-1α mediates PLGC and summarize the potential applications of TCM in the prevention and treatment of PLGC, aiming to provide a clear molecular framework for TCM intervention in PLGC and offer theoretical support and research directions for the development of innovative HIF-1α-targeted Chinese medicines.
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