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.