紫草素调控PTEN/AKT/TFEB信号通路改善心肌梗死大鼠心室重构OA

Objective To investigate the mechanism by which shikonin(SK)improves ventricular remodeling in myocardial infarc-tion(MI)by modulating the phosphatase and tensin homolog(PTEN)/protein kinase B(AKT)/transcription factor EB(TFEB)signaling pathway.Methods SD rats were randomly divided into Sham,MI,L-SK,H-SK,and H-SK+BpV groups(n=10 each).Cardiac function,myocardial histopathology,serum inflammatory factor levels,and protein expressions were assessed via echocardiography,histological staining,ELISA,and Western blotting.Results Compared with Sham group,MI group exhibited increased myocardial fibrosis,inflamma-tory infiltration,and deteriorated cardiac function.Compared with the MI group,SK-treated groups(L-SK,H-SK)showed reduced myocar-dial injury and fibrosis,and improved cardiac function in a dose-dependent manner,along with significant changes in PTEN/AKT/TFEB and autophagy-related proteins.The H-SK+BpV group demonstrated opposite trends.Conclusion SK may improve cardiac function and attenuate myocardial injury and fibrosis in MI rats by modulating the PTEN/AKT/TFEB signaling pathway,suppressing inflammation,and activating cardiomyocyte autophagy.