H [Formula: see text] S attenuates the myocardial fibrosis in diabetic rats through modulating PKC-ERK1/2MAPK signaling pathway

OBJECTIVE: To investigate the roles and underlying mechanism of exogenous H [Formula: see text] S (hydrogen sulfide) in attenuating the myocardial fibrosis in diabetic rats. METHODS: A total of 40 SD rats were randomly divided into 4 groups: control group, STZ group, STZ [Formula: see text] H [Formula: see text] S group and H [Formula: see text] S group. To build the DM rat model , the rats in the STZ group and STZ [Formula: see text] H [Formula: see text] S group were injected streptozotocin (STZ) intraperitoneally, While the rats in the STZ [Formula: see text] H [Formula: see text] S group and the H [Formula: see text] S group received sodium hydrosulfide (NaHS), which provides exogenous H [Formula: see text] S. Eight weeks later, the myocardial tissues of rats were used to detecting the collagen deposition through Masson staining, as well as some protein expressions related to myocardial fibrosis and signaling pathway by western blotting. RESULTS: Comparing to control group, the collagen deposition of myocardial matrix remarkably increased in the STZ group, and almost all the proteins that are relative to myocardial fibrosis, inflammatory and signaling pathway show an overexpression, except for PPARG and NF- [Formula: see text] Bp65. When Compared with the STZ group, the collagen deposition was obviously attenuated in STZ [Formula: see text] H [Formula: see text] S group, as well as the protein expressions above-mentioned, While PPARG was up-regulated. CONCLUSION: The myocardial fibrosis in DM rats can be attenuated effectively by exogenous H [Formula: see text] S, and the underlying mechanism is likely to regulating PKC-ERK1/2MAPK signaling pathway, improving the MMPs/TIMPs expression dysregulation and inhibiting inflammatory reaction.