Crocin attenuates oxidative stress and inflammation in myocardial infarction induced by isoprenaline via PPARγ activation in diabetic rats

Abstract

Hyperglycemia induced oxidative stress and inflammation lead to development of diabetic cardiomyopathy. Diabetic patients are more at risk for myocardial infarction than non-diabetics. The current study has investigated the involvement of PPARγ activation in effects of crocin as a natural carotenoid against cardiac infarction in diabetic rats. Diabetes was induced in male Wistar rats by streptozotocin injection (55mg/kg, i.p) 15min after the administration of nicotinamide (110mg/kg). Then saline, crocin (40mg/kg, orally) and GW9662 (1mg/kg, as PPARγ antagonist) were injected for 4weeks. Isoprenaline was administrated on the 27th and 28th days to induce infarction. Cardiac injury markers, antioxidant enzymes content, blood glucose level, lipid profile, pro and anti-inflammatory cytokines, and PPARγ gene expression were measured. GSH, CAT content, CK-MB isoenzyme, LDH level, IL-10 and PPARγ gene expression in myocardial tissue were decreased in diabetic rats receiving isoprenaline and inflammatory cytokines TNFα and IL-6 and also plasma lipids were increased. Crocin administration significantly ameliorated inflammatory cytokines levels, CK-MB, and LDH contents and also it could enhance antioxidant capacity and PPARγ expression. However, GW9662 administration reversed the effects of crocin. Overexpression of PPARγ in crocin treated rats and inhibition of crocin effects by GW9662 reflected the potential involvement of PPARγ pathway in the protective effects of crocin.