Abstract:
AIM: To explore the effects of arctiin ameliorates glucolipid metabolism and myocardial fibrosis in high-fat diet-induced insulin-resistant obese mice. METHODS: 45 male C57BL/6J mice were randomly divided into normal diet group(ND,10 kcal% Fat), high-fat diet group(HFD,60 kcal% Fat).The HFD group that established insulin-resistant was randomly divided into: HFD group, HFD+CMC-Na group, HFD+Arctiin group. Arctiin treatment with 100, 200mg/(kg·d) for 10 weeks, oral gavage, CMC-Na was used as the vehicle. After 10 weeks, blood lipid and glucose levels were measured. HE and Masson staining were used to detect the morphology and fibrosis of myocardial. RT-qPCR and WB were used to detect the expression of Collagen I, Collagen III, AUF1, TGF-β1/Smad3 signaling Pathway. RESULTS: Compared with ND group, the levels of low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), and triglycerides (TG) in HFD group were significantly increased; Fasting blood glucose (FBG) ,Fasting insulin ( FIN), and HOMA-IR were increased; Collagen I, Collagen III, AUF1,TGF-β1/Smad3 signaling Pathway expression were significantly increased. Compared with HFD group, the indicators in HFD+CMC-Na group were shown no statistical significance; the levels of TC and TG in HFD+ARC group were decreased; FBG, FIN and HOMA-IR were decreased, especially in high dose. The expression levels of Collagen I, Collagen III, AUF1, TGF-β1/Smad3 signaling Pathway were reduced. CONCLUSION: Arctiin can regulate glucolipid metabolism, ameliorate insulin resistance, reduce myocardial collagen secretion, and improve myocardial fibrosis. Its mechanism may be connected with the inhibition of AUF1 and TGF-β1/Smad3 pathway.