Abstract
Background and Objective. High-cholesterol diet (HCD) intends to increase the oxidative stress in liver tissues inducing hepatotoxicity. Rutin is a natural flavonoid (vitamin p) which is known to have antioxidative properties. The aim of the present study was to investigate the potential effects of Rutin on hypercholesterolemia-induced hepatotoxicity in rats. Materials and Methods. Male Wistar rats were divided into four groups: G-I control, G-II Rutin, G-III HCD, and G-IV Rutin + HCD. The liver functions and lipid profile were used to evaluate the HCD-induced hepatotoxicity. Quantitative real time-PCR was carried out to evaluate the expression levels of genes in TGF-β/Smad signaling pathway. Results. Rutin in combination with HCD showed a significant protective effect against hepatotoxicity. HCD caused significant increase in the mRNA expression of transforming growth factor beta (TGF-β), Mothers Against Decapentaplegic Homolog 2 (Smad-2), Mothers Against Decapentaplegic Homolog 4 (Smad-4), Bcl-2-binding component 3 (Bbc3), caspase-3, P53 and Interleukin-6 (IL-6) and decrease in the expression levels of Cyclin depended kinase inhibitor (P21) and Interleukin-3 (IL-3) in hepatic cells. Conclusion. TGF-β/Smad signaling pathway is involved in HCD-induced hepatotoxicity and Rutin inhibits the hepatotoxicity via suppressing this pathway. Therefore, Rutin might be considered as a protective agent for hepatotoxicity.
Highlights
Nonalcoholic steatohepatitis (NASH) is a form of chronic liver disease and a part of nonalcoholic fatty liver disease (NAFLD), which may lead to cirrhosis and hepatocellular carcinoma (HCC) [1,2,3,4,5,6,7]
Oxidative stress induced by high-cholesterol diet can mediate a variety of cellular responses leading to diverse outcomes such as apoptosis [10, 11], which is involved in NASH causation [12]
Our findings demonstrated that Rutin could lower and attenuate hepatotoxicity induced by High-cholesterol diet (HCD) in rat model
Summary
Nonalcoholic steatohepatitis (NASH) is a form of chronic liver disease and a part of nonalcoholic fatty liver disease (NAFLD), which may lead to cirrhosis and hepatocellular carcinoma (HCC) [1,2,3,4,5,6,7]. Oxidative stress induced by high-cholesterol diet can mediate a variety of cellular responses leading to diverse outcomes such as apoptosis [10, 11], which is involved in NASH causation [12]. High-cholesterol diet (HCD) intends to increase the oxidative stress in liver tissues inducing hepatotoxicity. The aim of the present study was to investigate the potential effects of Rutin on hypercholesterolemia-induced hepatotoxicity in rats. The liver functions and lipid profile were used to evaluate the HCD-induced hepatotoxicity. Rutin in combination with HCD showed a significant protective effect against hepatotoxicity. HCD caused significant increase in the mRNA expression of transforming growth factor beta (TGF-β), Mothers Against Decapentaplegic Homolog 2 (Smad-2), Mothers Against Decapentaplegic Homolog 4 (Smad-4), Bcl2-binding component 3 (Bbc3), caspase-3, P53 and Interleukin-6 (IL-6) and decrease in the expression levels of Cyclin depended kinase inhibitor (P21) and Interleukin-3 (IL-3) in hepatic cells. Rutin might be considered as a protective agent for hepatotoxicity
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