This study aims to investigate the role and regulatory mechanism of the Hydrogen sulfide (HS) in amelioration of rat myocardial fibrosis induced by thyroxine through interfering the autophagy via regulating the activity of PI3K/AKT1 signaling pathway and the expression of relative miRNA. 40 adult male SD rats were randomly divided into 4 groups (n = 10): the control group， the thyroxine model group (TH group)， the model group with HS intervention (TH + HS group) and the normal group with HS intervention (HS group). Pathological changes were observed via H&E staining and Masson staining， Expressions of MMPs/TIMPs， PI3K/AKT， autophagy-related proteins in myocardial tissues were detected via Western blot... More
This study aims to investigate the role and regulatory mechanism of the Hydrogen sulfide (HS) in amelioration of rat myocardial fibrosis induced by thyroxine through interfering the autophagy via regulating the activity of PI3K/AKT1 signaling pathway and the expression of relative miRNA. 40 adult male SD rats were randomly divided into 4 groups (n = 10): the control group， the thyroxine model group (TH group)， the model group with HS intervention (TH + HS group) and the normal group with HS intervention (HS group). Pathological changes were observed via H&E staining and Masson staining， Expressions of MMPs/TIMPs， PI3K/AKT， autophagy-related proteins in myocardial tissues were detected via Western blotting， and the expressions of miR-21， miR-34a， miR-214 and miR-221 were detected via RT-qPCR. Compared with the control group， in the TH group， myocardial fibrosis was more significant， the expressions of proteins in PI3K/AKT and autophagy-related proteins were significantly decreased， as well as the expression of miR-221; while the expressions of miR-21， miR-34a and miR-214 were significantly elevated. By contrast， all above-mentioned changes were obviously reversed with HS treatment， which demonstrated the positive function of HS in amelioration of rat myocardial fibrosis induced by thyroxine. The mechanism of such amelioration may be correlated with autophagy activated by the upregulation of expression of PI3K/AKT signaling pathway and downregulation of expressions of miR-21， miR-34a and miR-214.
