Autophagy And Salidroside Intervention Of The Smooth Muscle Cells Of The Cavernosa Of The Penis In Erectile Dysfunction Rats With Cavernous Nerve Injury

Objective 1.To explore the effects of salidroside on apoptosis and autophagy of corpus cavernosum smooth muscle cells(CCSMCs)under oxidative stress in vitro;2.To explore the changes of apoptosis and autophagy of penile corpus cavernosum and treatment effect of salidroside in SD rats with ED under bilateral cavernous nerve injury.Methods 1.Cultured primary CCSMCs in vitro were exposed to hydrogen peroxide(H2O2)to simulate an oxidative stress environment in vitro.Cell viability was measured using the CCK-8 method.Oxidative stress levels were detected by ROS,MDA,SOD,and apoptosis was detected using DAPI staining and Western Blotting was used to detect Bax and Bcl-2 proteins.Western Blotting,immunofluorescence,and electron microscopy were used to observe autophagy,while interventions were used to observe the effects of salidroside.2.Forty SD rats were randomly divided into 4 groups,which were respectively subjected to sham surgery,bilateral CN crush injury,salidroside treatment group,and rapamycin autophagy activation positive control group.After 3 weeks of treatment,the penile hemodynamics used electrical stimulation of the cavernous nerve to measure the intracavernosal pressure(ICP).After collecting the penile cavernous tissue and weighing it,detected by HE,Masson’s staining,Western Blotting,electron microscopy,tissue immunofluorescence,and histochemical detection.Death,autophagy,apoptosis-related proteins and autophagosomes,endothelial cells and smooth muscle content,as well as dorsal nerve nNOS indicators.Results 1.The primary isolated CCSMCs were spindle-shaped,and smooth muscle marker α-SMA and Desmin were positive for fluorescent staining.Salidroside restored cytotoxicity,oxidative stress,and apoptosis after H2O2 treatment.Salidroside enhances autophagy-related proteins(LC3-II,Beclin-1).When using autophagy inhibitor 3-methyladenine(3-MA)to block autophagy,the therapeutic effect of salidroside completely disappeared.Conclusion 1.Salidroside can activate protective autophagy of CCSMCs and improve apoptosis induced by oxidative stress;2.Salidroside may inhibit the degree of apoptosis and fibrosis in the cavernous body by activating protective autophagy to improve the ED after bilateral CN injury.