Effects of hydrogen sulfide on myocardial fibrosis and MAPK1/3 and MMP-8 expression in diabetic rats.
- Author:
Fang LI
1
;
Ou ZENG
;
Jian LUO
;
Zhi-Xiong WU
;
Ting XIAO
;
Jing-Jing ZHANG
;
Jun YANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Collagen Type I; metabolism; Diabetes Mellitus, Experimental; metabolism; pathology; Fibrosis; Hydrogen Sulfide; pharmacology; Injections, Intraperitoneal; Male; Matrix Metalloproteinase 8; metabolism; Mitogen-Activated Protein Kinase 1; metabolism; Mitogen-Activated Protein Kinase 3; metabolism; Myocardium; pathology; Rats; Rats, Sprague-Dawley
- From: Journal of Southern Medical University 2015;35(4):549-552
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effects of hydrogen sulfide (H(2)S) on myocardial fibrosis and expressions of MAPK1/3 and MMP-8 in diabetic rats.
METHODSForty adult male SD rats were randomized into 4 groups, namely the control group, diabetes mellitus group (STZ group), diabetes mellitus with H(2)S treatment group (STZ+H(2)S group), and normal rats with H(2)S treatment group (H(2)S group). Diabetes was induced by intraperitoneal injections of 40 mg/kg streptozotocin (STZ). The rats in the control group received daily intraperitoneal injections of saline, and those in STZ+H(2)S group and H(2)S group were given NaHS (100 µmol/kg) injections. After 8 weeks, the pathologies of cardiac fibrosis were examined with HE staining, and the expressions of collagen I, MAPK1/3 and MMP-8 were analyzed with Western blotting.
RESULTSCompared with the control group, the diabetic rats showed increased collagen content and obvious interstitial fibrosis in the myocardial tissue with significantly increased expression levels of collagen I, MAPK1/3 and MMP-8 (P<0.05); all these changes were obviously reversed by treatment with H(2)S (P<0.05). Collagen I, MAPK1/3 and MMP-8 expression levels and the degree of myocardial fibrosis were comparable between H(2)S group and control group (P>0.05).
CONCLUSIONHydrogen sulfide can attenuate cardiac fibrosis in diabetic rats, and the mechanism may involve the inhibition of MAPK1/3/MMP-8 signal pathway.
