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Streptozotocin (STZ)-induced diabetes mellitus (DM) model shows the signal of cardiac dysfunction,which is manifested as myocardial fibrosis and hypertrophy. This study was designed to predict targetsof sodium hydrosulfide (NaHS) for diabetic cardiomyopathy and its corresponding triggered pathwaysby network pharmacology analysis and test the effects of NaHS as well as its mechanism as possiblemodulators of left ventricular remodeling in diabetic rats. The drug-target networks were constructed viaapproaches of network pharmacology, and the predicted targets and pathways were validated by in vivoexperiments. Rats were randomly divided into 3 groups (n=6/group): STZ-induced DM group (STZDM); STZ-induced DM treated with H2S group (STZ-NaHS); control group. The control group wastreated with daily saline (i.p.); the diabetic model was induced by intraperitoneal (i.p.) injections of 40mg/kg/day STZ. After 12 weeks, the rat cardiac function was determined, and the pathologicalmorphology of the heart was analysed by Masson trichrome staining in each group. The expression levelof matrix metalloproteinase 9 (AGEs), CSE, CBS and several autophagy associated proteins weredetected by the ELISA analysis. Results from the PPI network implied that 27 targets were key regulators.The AGE-RAGE signaling pathway in diabetic complications and the apoptotic signaling pathway wasdiscovered to be the key to anti-diabetic cardiomyopathy of NaHS upon the GO enrichment analyses andKEGG pathway. In the in vivo experiment, compared with the control group, cardiac fibrosis andattenuated left ventricular function were observed. Furthermore, compared with the control group, theexpression level of CSE, CBS and autophagy associated proteins Atg5 was significantly decreased, whilethat of AGEs, autophagy associated proteins p62 and p-ERK1/2 was significantly increased in the STZDM group (P&lt;0.05). In the STZ-NaHS group, cardiac fibrosis and ventricular dysfunction wereameliorated, the expression level of CSE, CBS and autophagy associated proteins Atg5 was increased,and the expression level of AGEs, autophagy associated proteins p62 and p-ERK1/2 was significantlydecreased (P&lt;0.05). In conclusion, H2S may alleviate cardiac fibrosis of the STZ-induced DM rat modelby enhancing cardiac autophagy, inhibiting cardiomyocyte apoptosis and downregulating p-ERK1/2.

journal of diabetes, metabolism and its complications

Exogenous Hydrogen Sulfide Alleviated Left Ventricular Fibrosis Via Enhancing Cardiac Autophagy and Decreasing Cardiomyocyte Apoptosis in StreptozotocinInduced Diabetic Rats: From Network Pharmacology to Experimental Pharmacology