Comparison of the anti-inflammatory and antilipidemic activity of diosmin and saroglitazar in a model of nonalcoholic fatty liver induced by a high-fat diet in Wistar rats
- سال انتشار: 1403
- محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 27، شماره: 2
- کد COI اختصاصی: JR_IJBMS-27-2_014
- زبان مقاله: انگلیسی
- تعداد مشاهده: 171
نویسندگان
Hyperlipidemia Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Hyperlipidemia Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Hyperlipidemia Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Hyperlipidemia Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Hyperlipidemia Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Student Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Diabetes Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
چکیده
Objective(s): Non-alcoholic fatty liver disease (NAFLD) is the most common liver-related metabolic disorder in the world, with a global prevalence of ۲۵%. Compounds with anti-inflammatory, lipid-lowering, and insulin-sensitizing properties can be used for the prevention or treatment of NAFLD. Therefore, this study was conducted to investigate the effect of saroglitazar (a dual PPARα/γ agonist) and diosmin (a flavonoid) on non-alcoholic fatty liver induced by a high-fat diet (HFD) in Wistar rats.Materials and Methods: Forty male Wistar rats (۶–۸ weeks old) were fed an HFD to induce NAFLD. After ۷ weeks, rats were divided into four groups: group۱ was fed HFD, and the other groups received HFD+saroglitazar, HFD+diosmin, and HFD+ saroglitazar+diosmin. We examined body and liver weight, histopathology, serum levels of liver enzymes (ALT and AST), and lipid profiles (LDL-C and HDL-C) using the standard protocols. qRT-PCR was also used to examine the expression of PPARα, PPARγ, SREBP۱c, FAS, ACC, CPT۱α, and pro-inflammatory genes (IL۶, TNFα, and TGFβ). Results: Rats fed the HFD showed characteristics of NAFLD (pathologically and biochemically). Administration of saroglitazar and diosmin alone caused a significant decrease in the levels of PPARγ, SREBP۱c, FAS, ACC, ALT, AST, LDL-C, and pro-inflammatory genes and a significant increase in PPARα, CPT۱a, and HDL-C in comparison with the HF group (P< ۰.۰۵). Their combined effect was more evident. Conclusion: Our results showed that diosmin, like saroglitazar, significantly ameliorated inflammatory and lipid profiles in HFD-induced NAFLD, suggesting that diosmin, as a natural compound, could be a suitable alternative to saroglitazar.کلیدواژه ها
Diosmin, Non-alcoholic fatty liver disease, Non-alcoholic steatohepatitis, Saroglitazar, TGFβاطلاعات بیشتر در مورد COI
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