Mohammad Badavi 1,2 , Seyyed Ali Mard 1,2,3 , Mahin Dianat 1,2 , Neda Dashtbozorgi 1,2 Show Affiliations »
Abstract
BACKGROUND AND PURPOSE: 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. MATERIALS AND METHODS: Diabetes was induced in male Wistar rats by streptozotocin injection (55 mg/kg, i.p) 15 min after the administration of nicotinamide (110 mg/kg). Then saline, crocin (40 mg/kg, orally) and GW9662 (1 mg/kg, as PPARγ antagonist) were injected for 4 weeks. 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. RESULTS: 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. CONCLUSION: 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. © Springer Nature Switzerland AG 2020.
BACKGROUND AND PURPOSE: 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. MATERIALS AND METHODS: Diabetes was induced in male Wistar rats by streptozotocin injection (55 mg/kg, i.p) 15 min after the administration of nicotinamide (110 mg/kg). Then saline, crocin (40 mg/kg, orally) and GW9662 (1 mg/kg, as PPARγ antagonist) were injected for 4 weeks. 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. RESULTS: 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. CONCLUSION: 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. © Springer Nature Switzerland AG 2020.
Entities: Chemical
Keywords:
Crocin; Inflammation; Myocardial infarction; PPARγ; Rat
Year: 2020
PMID： 33553037 PMCID： PMC7843838 DOI： 10.1007/s40200-020-00686-y
Source DB: PubMed Journal: J Diabetes Metab Disord ISSN： 2251-6581