参萸养心胶囊对心肌纤维化小鼠的影响及作用机制OACHSSCD

Objective:To evaluate the efficacy,targets,and mechanisms of Shenyu Yangxin Capsules on myocardial fibrosis(MF)in mice.Methods:Fifty male C57BL/6J mice were randomly assigned to five groups(n=10 each)according to a random number table:control group,model group,low-and high-dose Shenyu Yangxin Capsules group(1 and 2 mg/d for capsule contents in freeze-dried powder),and captopril group(0.2 mg/d).Except for the control group,mice in all other groups were injected subcutaneously with isoproterenol(5 mg/kg)once daily for 14 days to induce MF.On the day of model establishment,the low-and high-dose She-nyu Yangxin Capsules groups and the captopril group received oral administration,while the control and model groups received an equal volume of distilled water.After 14 days of treatment,cardiac function was assessed by ultrasound,measuring left ventricular e-jection fraction(LVEF)and left ventricular fractional shortening(LVFS).MF was evaluated by Masson's trichrome staining.Immu-nohistochemistry was performed to detect protein expression of transforming growth factor-β1(TGF-β1),alpha-smooth muscle actin(α-SMA),and collagen Ⅲ(Col Ⅲ)in myocardial tissue.Real-time PCR was used to measure mRNA expression of interleukin-6(IL-6),TGF-β1,α-SMA,and Col Ⅲ.Western blot analysis was performed to detect protein levels of TGF-β1,α-SMA,Smad3,and phospho-Smad3(p-Smad3).Results:Compared with the control group,mice in the model group exhibited significantly reduced LVEF and LVFS,increased myocardial collagen volume fraction and collagen-positive area(P＜0.01),and significantly elevated mRNA expression of IL-6,TGF-β1,α-SMA,and Col Ⅲ(P＜0.01),as well as protein levels of TGF-β1,α-SMA,Smad3,and p-Smad3(P＜0.01).Compared with the model group,the captopril group and both Shenyu Yangxin Capsules groups showed varying degrees of improvement in all the above indicators,with all differences statistically significant(P＜0.01).Conclusion:Shenyu Yangxin Capsules ameliorates isoproterenol-induced cardiac dysfunction,reduces collagen deposition,and delays the progression of MF in mice,potentially by inhibiting the TGF-β1/Smad3 signaling pathway.