Latest ArticlesDiabetic kidney disease (DKD) is the most common and severe microvascular complication in clinical practice and one of the main causes for diabetic patients to develop chronic kidney disease and end-stage renal disease. The pathogenesis of this disease involves the combined effects of multiple factors, such as genetic factors, dysregulation of glucose and lipid metabolism, changes in renal hemodynamics, inflammatory responses and oxidative stress, among others. Among these, oxidative stress is the core process in the occurrence and development of DKD. The nuclear transcription factor E2-related factor (Nrf2) is an important regulatory factor for antioxidant stress transcription. Activating Nrf2 can stimulate the expression of downstream heme oxygenase-1 (HO-1), thereby widely participating in various biological processes such as regulating oxidative stress, reducing inflammatory responses and inhibiting cell apoptosis in the body. Recent studies have shown that the Nrf2/HO-1 signaling pathway is involved in the occurrence, development and drug intervention process of DKD. Traditional Chinese medicine (TCM) has the characteristics of multi-target, multi-pathway and multi-level, and the advantages of synergism and attenuation, showing unique advantages in making up for the shortcomings of modern medicine. However, there is still a lack of systematic summary of the mechanism of this pathway in the prevention and treatment of DKD and the research progress of traditional Chinese medicine. In this paper, the biological function and activation process of Nrf2/HO-1 pathway, the relationship between Nrf2/HO-1 pathway and DKD, the related research of traditional Chinese medicine to improve DKD by targeting the pathway in recent years, the treatment strategy of integrated traditional Chinese and western medicine, and the future research direction were systematically reviewed, in order to provide theoretical reference for the clinical treatment and drug development of DKD.
To analyze the application effect of the intelligent management system for clinical trial drugs.
Based on the overall architecture established for the intelligent module and the management of experimental drugs, we compared the error rates of monthly prescriptions and recovery forms from 2024 to 2025, as well as the error rates of annual prescriptions and recovery forms from 2024 to 2025.
The prescription error rates for January 2024 and 2025 were 33.33% (4 prescriptions/12 prescriptions) and 0% (0 prescriptions/19 prescriptions), respectively; for May, they were 30.00% (6 prescriptions/20 prescriptions) and 5.56% (2 prescriptions/36 prescriptions), respectively; for June, they were 36.00% (9 prescriptions/25 prescriptions) and 3.21% (6 prescriptions/187 prescriptions), respectively; for July, they were 23.91% (11 prescriptions/46 prescriptions) and 5.14% (9 prescriptions/175 prescriptions), respectively; for August, they were 10.71% (6 prescriptions/56 prescriptions) and 1.82% (3 prescriptions/165 prescriptions), respectively; for September, they were 10.20% (10 prescriptions/98 prescriptions) and 2.84% (5 prescriptions/176 prescriptions), respectively; for October, they were 13.21% (7 prescriptions/53 prescriptions) and 2.70% (2 prescriptions/74 prescriptions), respectively; for December, they were 12.50% (6 prescriptions/48 prescriptions) and 3.02% (13 prescriptions/430 prescriptions), respectively. The above indicators were statistically significant differences between the two groups (P<0.05, P<0.01). The prescription error rates for the years 2024-2025 were 12.41% (82 prescriptions/661 prescriptions) and 3.38% (60 prescriptions/1 777 prescriptions), respectively, showing a downward trend, and there were statistically significant differences between the two groups(P<0.000 1). The overall error rate of the collected forms decreased, but differences were not statistically significant (P>0.05).
The intelligent management system can improve the efficiency and accuracy of drug management, and it is recommended to further optimize the recovery process.
To investigate the effects and mechanism of naringenin inhibiting the non-receptor tyrosine kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway on the proliferation and apoptosis of esophageal cancer cells.
The effects of different doses of naringenin on KYSE150 cell viability was screened using cell counting kit-8 (CCK-8), and naringenin concentration was selected. KYSE150 cells were sequentially divided into control group (conventional culture), low-dose experimental group (10 μmol·L-1 naringenin), high-dose experimental group (40 μmol·L-1 naringenin), JAK2/STAT3 pathway inhibitor group (20 μmol·L-1 AG490) and JAK2/STAT3 pathway activator group (40 μmol·L-1 naringenin and 10 μmol·L-1 coumermycin A1). The 5-bromo-2 ’- deoxyuridine (Brdu) positive cell rate was detected using the Brdu staining method, the number of cell clones formed was detected using the clone formation assay, the expression of proliferation and apoptosis related genes was detected using reverse transcription real-time fluorescence quantitative polymerase chain reaction (RT-qPCR), the apoptosis rate was detected using flow cytometry, the terminal deoxynucleotide transferase mediated 2’-deoxyuridine-5’- triphosphate notch end labeling (TUNEL) positive rate was detected using the TUNEL staining method, the expression of JAK2/STAT3 pathway related proteins was detected using Western blot, and the effect of naringenin on the growth of KYSE150 xenograft tumors Ki-67 nuclear antigen (Ki67) and tumor tissues growth in nude mice was detected using immunohistochemistry.
The half maximal inhibitory concentration of naringenin on KYSE150 cell viability is close to 40 μmol·L-1. The Brdu positivity rates of KYSE150 cells in control group, low-dose experimental group, high-dose experimental group, JAK2/STAT3 pathway inhibitor group and JAK2/STAT3 pathway activator group were (58.64±5.23)%, (46.23±4.05)%, (21.05±3.04)%, (23.62±3.15)% and (35.98±3.21)%, respectively; the clone formation numbers were (102.36±10.25), (78.64±7.21), (50.05±4.32), (52.39±5.03) and (61.55±5.12) cells, respectively; the relative expression levels of CyclinB1 messenger ribonucleic aeid (mRNA) were 1.02±0.11, 0.74±0.05, 0.45±0.04, 0.48±0.05 and 0.62±0.06, respectively; the relative expression levels of cyclin dependent kinase 1 (CDK1) mRNA were 1.03±0.07, 0.62±0.05, 0.27±0.03, 0.30±0.04 and 0.51±0.04, respectively; the apoptosis rates were (4.15±0.42)%, (15.62±1.02)%, (29.65±2.03)%, (27.84±1.98)% and (19.66±1.20)%, respectively; the positive rates of TUNEL were (8.65±0.82)%, (20.64±2.03)%, (37.68±3.05)%, (35.62±2.16)% and (28.14±2.01)%, respectively; the relative expression levels of Bcl-xl mRNA were 1.02±0.07, 0.72±0.06, 0.41±0.04, 0.44±0.05 and 0.59±0.05, respectively; the relative expression levels of Bcl-2 mRNA were 1.01±0.05, 0.59±0.04, 0.36±0.03, 0.39±0.04 and 0.50±0.03, respectively. Compared control group with low-dose experimental group, high-dose experimental group and JAK2/STAT3 pathway inhibitor group, compared low-dose experimental group with high-dose experimental group and JAK2/STAT3 pathway inhibitor group, compared high-dose experimental group with JAK2/STAT3 pathway activator group, the above indicators all showed statistically significant differences (all P<0.05). In nude mouse experiments, the tumor volumes of animal control group, animal low-dose experimental group and animal high-dose experimental group were (1 287.65±98.54), (821.22±71.65) and (425.39±37.69) mm3, respectively; the tumor masses were (1.85±0.12), (1.20±0.09) and (0.73±0.05) g, respectively; the Ki67 positivity rates in tumor tissues were (69.52±5.36)%, (44.35±3.12)% and (20.06±2.85)%, respectively. The above indicators of the animal low and high-dose experimental groups were statistically significantly different from those of animal control group, and the above indicators of the animal high-dose experimental group were statistically significantly different from those of animal low-dose experimental group (all P<0.05).
Naringenin clearly inhibits the proliferation and promotes apoptosis of esophageal cancer KYSE150 cells by suppressing the JAK2/STAT3 signaling pathway.
Heart failure (HF) refers to a clinical syndrome caused by structural or functional cardiac disorders that impair ventricular filling and/or ejection function, resulting in insufficient cardiac output to meet the metabolic demands of bodily tissues. Its clinical manifestations include congestion in the pulmonary and/or systemic circulation, as well as inadequate blood perfusion to organs and tissues. As the terminal stage of various cardiovascular diseases, HF ranks among the leading causes of death for urban and rural residents in China. microRNA (miRNA) is a class of endogenous non-coding single-stranded ribonucleic acids (RNAs) that regulate gene expression at the post-transcriptional level. They are involved in multiple pathological processes of HF, such as myocardial remodeling, cell death, energy metabolism and inflammatory immunity, thus exhibit potential as therapeutic targets for the disease. Traditional Chinese medicine (TCM), characterized by multi-targeted and multi-pathway actions, has shown unique advantages in the prevention and treatment of HF by modulating miRNAs. This article reviews the recent research status on miRNA-mediated regulation of HF and the mechanisms underlying TCM interventions, with the aim of providing insights for subsequent HF-related studies.
To investigate the effect and mechanism of dihydroartemisinin (DHA) on ferroptosis in cervical cancer by the microRNA (miRNA)-346/Kruppel-like factor 14 (KLF14) axis.
In cell experiment, human cervical cancer Hela cells were treated and divided into several groups including cell normal control group (only HcerEpic cell), cell negative control group (only Hela cell), cell experimental group (Hela cell treated with 246.90 μmol·L-1 DHA for 48 h), DHA+mimic NC group (transferred with mimic NC based on the cell experimental group), DHA+miR-346 mimic group (transfected with miRNA-346 mimic based on the cell experimental group), DHA+sh-NC group (transfected with sh-NC based on the cell experimental group) and DHA+sh-KLF14 group (transfected with sh-KLF14 based on the cell experimental group). In animal experiment, a xenograft tumor model was established by subcutaneous injection of Hela cells into 30 female BALB/c nude mice, which were then divided into the animal control group (gavaged with saline), animal experimental-L group (gavaged with 100 mg·kg-1 DHA) and animal experimental-H group (gavaged with 200 mg·kg-1 DHA), with 10 mice in each group. The relative expression level of miRNA-346 was detected by quantitative real-time polymerase chain reaction. The relative expression levels of KLF14 protein, glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) were measured by Western blot. Intracellular Fe2+ levels were detected using FerroOrange fluorescent probe. The apoptosis rate was determined by the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay.
In cell experiment, the relative expression levels of miRNA-346 in the cell negative group and cell experimental group were 1.00±0.18 and 0.42±0.06, respectively; the relative expression levels of KLF14 mRNA were 1.00±0.17 and 2.22±0.32, respectively; the relative expression levels of KLF14 protein were 1.00±0.15 and 1.72±0.23, respectively; the relative fluorescence intensities of Fe2+ of cell negative control group, cell experimental group, DHA+mimic NC group, DHA+miRNA-346 mimic group, DHA+sh-NC group and DHA+sh-KLF14 group were 1.00±0.15, 4.86±0.81, 4.32±0.62, 3.12±0.57, 4.23±0.59 and 2.02±0.33, respectively; the relative expression levels of GPX4 protein were 1.00±0.17, 0.45±0.06, 0.48±0.07, 0.78±0.11, 0.44±0.06 and 0.59±0.08, respectively; the relative expression levels of SLC7A11 protein were 1.00±0.12, 0.37±0.05, 0.35±0.04, 0.86±0.12, 0.40±0.07 and 0.77±0.10, respectively; the cell proliferation rates were (100.00±3.65)%, (54.32±7.65)%, (56.32±8.02)%, (72.33±8.65)%, (52.32±9.23)% and (88.25±10.35)%, respectively; the apoptosis rates were (14.32±1.61)%, (61.33±8.25)%, (57.32±7.13)%, (32.44±5.37)%, (59.63±8.98)% and (23.88±3.49)%, respectively. Significant differences were observed in the aforementioned parameters when comparing the cell experimental group with the cell negative group, comparing the DHA + miRNA-346 mimic group with the DHA + mimic NC group, and comparing the DHA + sh-KLF14 group with the DHA + sh-NC group (P<0.01,P<0.001). In animal group, the tumor volumes in the animal control, experimental-L and experimental-H groups were (542.36±92.33), (402.85±92.28) and (295.52±60.56) mm3, respectively; the tumor masses were (1.55±0.33), (1.22±0.22) and(0.88±0.15)g, respectively; the relative positive levels of GPX4 were 1.00±0.18, 0.55±0.07 and 0.42±0.04, respectively; the relative positive levels of SLC7A11 were 1.00±0.16, 0.48±0.06 and 0.29±0.03, respectively. Significant differences were also detected between the animal experimenal-L, -H group and the animal control group (P<0.05, P<0.01, P<0.001).
DHA promotes ferroptosis in cervical cancer by the miRNA-346/KLF14 axis-mediated GPX4 signaling pathway.
To investigate the effect and mechanism of liraglutide on cisplatin-induced acute kidney injury in renal tubular epithelial (HK-2) cells.
HK-2 cells were randomly divided into control group, model group and experimental group. The control group was cultured conventionally, the model group was treated with 20 μmol·L-1 cisplatin reagent for 48 hours, and the experimental group was treated with 100 nM liraglutide reagent in addition to the model group for 48 hours. Cell proliferation activity was detected by cell counting kit-8 (CCK-8) method. Western blot was used to detect cysteine-aspartic acid protease 3 (Caspase 3), cleaved cysteine-aspartic acid protease 3(C-Caspase3), B cell lymphoma-2 (Bcl-2) associated X protein (BAX), nuclear factor E2 related factor 2 (Nrf-2), superoxide dismutase 2 (SOD2), heme oxygenase-1 (HO-1) and reference β-actin protein relative expression levels; the relative expression levels of kidney injury molecule-1 (Kim-1), BAX and Bcl-2 related messenger ribonucleic acid (mRNA) were detected by real-time fluorescent quantitative polymerase chain reaction, and cell apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dutP nick end labeling (TUNEL). Reactive oxygen species (ROS) levels were measured by superoxide anion fluorescent probe (DHE).
CCK-8 assay showed that 100 nmol·L-1 was the optimal intervention concentration of liraglutide. After 48 hours of intervention, the relative expression levels of K1M-1 mRNA in control group, model group and experimental group were 0.98±0.25, 56.23±23.25 and 2.61±0.79, respectively; BAX /Bcl-2 mRNA relative expression levels were 1.01±0.08, 15.47±3.01 and 5.41±0.54, respectively; the apoptosis rates were (5.60±0.40)%, (40.00±4.79)% and (6.40±0.87)%, respectively; the fluores cence value of positive rates of DHE were 1.95±0.03, 3.01±0.28 and 1.51±0.13, respectively; the relative expression levels of Nrf-2 protein were 0.80±0.01, 0.47±0.01 and 0.68±0.02, respectively; the relative expression levels of SOD2 protein were 0.96±0.04, 0.57±0.28 and 0.91±0.04, respectively; the relative expression levels of HO-1 were 1.01±0.08, 0.47±0.05 and 1.56±0.18, respectively. There were statistically significant differences in the above indicators between model group and control group, and between experimental group and model group (P<0.05, P<0.01, P<0.001, P<0.000 1).
Liraglutide can reduce the apoptosis rate and oxidative stress level of renal tubular epithelial cells in cisplatin-induced acute kidney injury, and increase the level of superoxide.
To investigate the mechanism of esketamine (Esk) ameliorating postpartum depression (PPD)-like behaviors in mice by regulating the two pore domain potassium channel (TWIK)-related K+ channel 1(TREK-1) to activate the brain-derived neurotrophic factor (BDNF)/tyrosine kinase receptor B (TrkB) pathway, and to provide experimental evidence for clarifying the pathogenesis of PPD and developing novel targeted therapeutic strategies.
A total of 50 C57BL/6J pregnant mice were randomly divided into five groups (n=10 per group): control group, model group, experimental group, oe-NC group and oe-TREK-1 group. A PPD model was established in pregnant mice using the chronic unpredictable mild stress (CUMS) method. The control group was given an equal volume of normal saline; the model group was given normal saline after CUMS modeling; the experimental group was intraperitoneally injected with Esk (5 mg·kg-1) once daily for 3 weeks after modeling; the oe-NC group was injected with lentivirus-encapsulated oe-NC by the tail vein before modeling and subsequent Esk administration; the oe-TREK-1 group was injected with lentivirus-encapsulated oe-TREK-1 by the tail vein before modeling and subsequent Esk administration. Depressive-like behaviors were evaluated using the sucrose preference test (SPT) and tail suspension test (TST). Hematoxylin-eosin (HE) staining and Nissl staining were used to observe the pathological morphology of hippocampal tissue; real-time fluorescent quantitative polymerase chain reaction and Western blotting were employed to detect the relative expression levels of TREK-1 in hippocampal tissue; enzyme-linked immunosorbent assay was utilized to measure the expression levels of serum sex hormones; immunohistochemistry was adopted to detect the expression of microglial marker proteins; Western blotting was used to determine the relative expression levels of endoplasmic reticulum stress-related proteins; immunofluorescence was applied to detect the relative expression levels of brain-derived neurotrophic factor (BDNF) and tyrosine protein kinase B (TrkB).
The sucrose preference rates in the control, model, experimental, oe-NC and oe-TREK-1 groups were (84.74±14.46)%, (19.08±2.86)%, (79.62±12.54)%, (80.15±11.38)% and (52.44±8.15)%, respectively; the immobility time ratios in the tail suspension test were (31.16±4.63)%, (75.38±14.62)%, (49.26±8.59)%, (48.97±7.82)% and (62.53±9.24)%, respectively; the relative expression levels of TREK-1 mRNA in the hippocampal tissues were 1.00±0.15, 2.87±0.45, 1.55±0.21, 1.56±0.19 and 2.18±0.36, respectively; the relative expression levels of TREK-1 protein were 1.00±0.16, 2.75±0.38, 1.86±0.27, 1.84±0.19 and 2.44±0.34, respectively; serum estradiol (E2) levels were (1 263.55±152.77), (638.16±78.32), (985.24±107.48), (981.67±106.34) and (752.33±116.45) pg·mL-1, respectively; progesterone (P) levels were (9.53±1.06), (3.48±0.59), (8.54±1.07), (8.47±1.04) and (5.62±1.02) ng·mL-1, respectively; prolactin (PRL) levels were (15.98±2.19), (29.31±4.62), (19.25±2.58), (19.88±2.67) and (23.47±3.46) ng·mL-1, respectively; the relative expression levels of Iba-1 protein in the hippocampus were 1.00±0.16, 0.35±0.05, 0.87±0.14, 0.85±0.13 and 0.61±0.11, respectively; the relative expression levels of GRP78 protein were 1.00±0.17, 1.58±0.16, 1.17±0.14, 1.09±0.18 and 1.35±0.17, respectively; the relative expression levels of CHOP protein were 1.00±0.14, 1.71±0.23, 1.13±0.16, 1.11±0.12 and 1.34±0.18, respectively; the relative expression levels of Cleaved caspase-12 protein were 1.00±0.16, 1.45±0.19, 1.19±0.13, 1.16±0.12 and 1.38±0.16, respectively; the relative fluorescence intensities of BDNF were 1.00±0.16, 0.38±0.06, 0.84±0.09, 0.83±0.11 and 0.64±0.08, respectively; the relative fluorescence intensities of TrkB were 1.00±0.17, 0.57±0.09, 0.92±0.14, 0.91±0.12 and 0.75±0.11, respectively. Statistically significant differences were observed in the above indicators between the model group and the control group, between the experimental group and the model group, and between the oe-TREK-1 group and the oe-NC group (P<0.05, P<0.01, P<0.001).
Esketamine can alleviate PPD-like behaviors in mice by inhibiting TREK-1 expression, regulating sex hormone balance, improving microglial function and endoplasmic reticulum stress, and thereby activating the BDNF/TrkB pathway.
To explore the mechanism of theaflavin improving the inflammatory response of intestinal epithelial cells in ulcerative colitis (UC) through regulating NOD-like receptor thermal protein domain associated protein 3 (NLRP3) / Caspase-1 signaling pathway mediated by astrocyte elevated gene 1 (AEG-1).
NCM460 cells were divided into control group (conventional culture of NCM460 cells without any intervention treatment, model group (treated with 1 mg·L-1 lipopolysaccharide in NCM460 cells for 24 hours), experimental group (treated with 64 μmol·L-1 theaflavin and 1 mg·L-1 lipopolysaccharide in NCM460 cells for 24 h), pcDNA3.1-NC group (after NCM460 cells were transfected with the pcDNA3.1-NC plasmid, treated with 64 μmol·L-1 theaflavin and 1 mg·L-1 lipopolysaccharide for 24 h) and pcDNA3.1-AEG-1 group (after NCM460 cells were transfected with the pcDNA3.1-AEG-1 plasmid, treated with 64 μmol·L-1 theaflavin and 1 mg·L-1 lipopolysaccharide for 24 h). Cell viability was detected by cell counting kit-8 method, cell invasion ability was detected by Transwell assay, cell migration ability was detected by cell scratch assay, and mRNA levels of AEG-1 and barrier damage-related proteins were detected by real-time fluorescence quantitative reverse transcription polymerase chain reaction. Western blotting was used to detect the expressions of AEG-1, apoptosis, barrier injury and NLRP3/Caspase-1 signaling pathway-related proteins and enzyme-linked immunosorbent assay was used to detect the contents of inflammatory factors.
The cell migration rate of the control group, model group, experimental group were (78.85±13.47)%, (19.32±3.15)% and (54.97±9.03)%, respectively. The levels of interleukin-6 (IL-6) in the control group, model group, experimental group, pcDNA3.1-NC group and pcDNA3.1-AEG-1 group were (0.49±0.07), (1.36±0.21), (0.64±0.09), (0.68±0.10) and (1.21±0.18) pg·L-1, respectively; the apoptosis rates were (8.26±1.47)%, (27.09±4.62)%, (14.51±2.18)%, (16.75±2.83)% and (22.68±3.56)%, respectively; the relative expression levels of B-cell lymphoma-2 (Bcl-2) protein were 1.00±0.16, 0.39±0.07, 0.71±0.12, 0.67±0.09 and 0.54±0.08, respectively; the relative expression levels of Bcl-2-associated X (Bax) protein were 1.00±0.19, 6.45±1.12, 3.90±0.64, 3.79±0.58 and 6.07±0.96, respectively; the mRNA levels of AEG-1 were 1.00±0.13, 4.35±0.76, 1.92±0.33, 2.08±0.32 and 3.26±0.57, respectively; the relative expression levels of AEG-1 protein were 1.00±0.17, 4.82±0.79, 2.07±0.34, 2.25±0.36 and 3.94±0.71, respectively; the mRNA levels of Zonula Occludens-1 (ZO-1) were 1.00±0.15, 0.37±0.06, 0.76±0.13, 0.79±0.14 and 0.51±0.09, respectively, while the mRNA levels of Occludin were 1.00±0.16, 0.29±0.05, 0.58±0.10, 0.52±0.09 and 0.37±0.06, respectively; the relative protein expression levels of NLRP3 were 1.00±0.19, 6.58±1.06, 2.71±0.43, 2.59±0.42 and 5.16±0.94, respectively; the relative protein expression levels of cleaved caspase-1 were 1.00±0.16, 5.26±0.93, 3.42±0.59, 3.65±0.64 and 5.09±0.87, respectively. When comparing the model group with the control group and the experimental group, and the pcDNA3.1-NC group with the pcDNA3.1-AEG-1 group, the differences in the above indicators were all statistically significant (P<0.01, P<0.001).
Theaflavin can improve the inflammatory response of LPS-induced UC intestinal epithelial cells and inhibit cell apoptosis, and has a protective effect on epithelial barrier function. The mechanism may be related to the down-regulation of AEG-1 expression and the inhibition of the NLRP3/Caspase-1 signaling pathway.
To investigate the effects of curcumin on ferroptosis and neurological deficit in mice with intracerebral hemorrhage (ICH) and to clarify its potential molecular mechanism.
A total of 40 mice were divided into sham group, model group, experimental group and inhibitor group, with 10 mice in each group. Intracerebral hemorrhage model in mice was established by tail vein autologous blood injection. The sham group was injected with the same amount of normal saline; in the model group, the model group was established and injected with the same amount of normal saline; the experimental group was intragastrically administered with 200 mg·kg-1 curcumin, and the inhibitor group was intraperitoneally injected with 5 mg·kg-1 secretory phosphoprotein 1 (SPP1) inhibitor solution on the basis of 200 mg·kg-1 curcumin. At the end of the treatment, Longa score was used to evaluate the neurological deficit; the serum levels of Fe2+, malondialdehyde (MDA) and superoxide dismutase (SOD) were detected by enzyme-linked immunosorbent assay (ELISA); the relative fluorescence intensity of reactive oxygen species (ROS) in brain tissue was detected by immunofluorescence method; the relative expression levels of B-cell lymphoma 2 (BCL-2), BCL-2-associated X protein (Bax), nuclear factor erythroid 2-related factor 2 (Nrf2) and glutathione peroxidase (GPX4) were detected by Western blot; the relative positive level of SPP1 in brain tissue was detected by immunohistochemistry.
The neurological deficit scores of sham group, model group, experimental group and inhibitor group were (0±0), (3.20±0.42), (1.40±0.52) and (2.10±0.57) scores, respectively; the serum Fe2+levels were (220.35±26.17), (432.40±65.28), (276.52±33.20) and (329.15±45.71) μmol·kg-1, respectively; the serum MDA levels were (53.75±7.62), (120.36±18.22), (72.68±11.23) and (89.44±13.16) nmol·mg-1, respectively; the serum SOD levels were (63.78±9.80), (20.86±3.41), (51.18±7.30) and (37.35±5.08) U·mg-1, respectively; the relative fluorescence intensities of ROS were 1.00±0.09, 3.87±0.56, 1.52±0.22 and 2.43±0.38, respectively; the relative expression levels of Bax in brain tissue were 1.00±0.11, 2.95±0.33, 1.58±0.26 and 2.37±0.29, respectively; the relative expression levels of Bcl-2 were 1.00±0.15, 0.20±0.04, 0.65±0.12 and 0.43±0.07, respectively; the relative expression levels of Nrf2 were 1.00±0.13, 0.33±0.05, 0.65±0.10 and 0.54±0.09, respectively; the relative expression levels of GPX4 were 1.00±0.14, 0.21±0.04, 0.58±0.09 and 0.45±0.06, respectively; the relative positive levels of SPP1 were 1.00±0.13, 0.30±0.05, 0.76±0.12 and 0.43±0.07, respectively. There were statistically significant differences in the above indicators between the model group and the sham operation group, between the experimental group and the model group, and between the inhibitor group and the experimental group (P<0.05, P<0.01, P<0.001).
Curcumin can alleviate neuronal apoptosis and ferroptosis after ICH, and improve neurological function injury in mice. The underlying mechanism may be associated with the up-regulation of SPP1 expression, which in turn activates the Nrf2/GPX4 signaling pathway.
Pharmacological treatment of bladder cancer (BC), including intravesical chemotherapy, systemic chemotherapy, chemoradiotherapy, and immunotherapy, still faces major challenges such as high recurrence rates, drug resistance, and treatment-related toxicities. As an important adaptive response under therapeutic stress, autophagy exerts a dual role in BC; it may cooperate with apoptosis and other pathways to mediate tumor cell death, or function as protective autophagy to promote cell survival and drive drug resistance. Therefore, strategies aimed at inducing lethal autophagy or inhibiting therapy-induced protective autophagy/autophagic flux blockade have emerged as potential approaches to optimize treatment response. Active components and compound formulas of traditional Chinese medicine can modulate autophagy through signaling pathways such as AMP-activated protein kinase/mechanistic target of rapamycin (AMPK/mTOR), and have shown potential to suppress tumor growth, enhance therapeutic sensitivity, and reduce toxicity. However, current evidence is still largely limited to in vitro and animal studies, criteria for autophagic flux evaluation remain inconsistent, and systematic studies on pharmacokinetics/pharmacodynamics (PK/PD), drug-drug interactions, and safety are lacking. Based on a systematic review of previous basic and preclinical studies, this article focuses on the representative molecular mechanisms by which active components and compound formulas of traditional Chinese medicine regulate autophagy, as well as their potential benefits and major limitations in the pharmacological treatment of BC, and further proposes possible directions for subsequent combination therapy and optimization of therapeutic strategies from the perspective of clinical pharmacology.
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