Abstract
Chronic alcohol intake leads to alcoholic fatty liver. The pathogenesis of alcoholic fatty liver is related to abnormal lipid accumulation, oxidative stress, endotoxins, and cytokines. Solanum muricatum Ait. (Pepino) is a plant food commonly cultivated in the Penghu island, Taiwan. Previous studies indicated that the aqueous extract of pepino was able to attenuate diabetic progression via its antioxidative and anti-inflammatory effects. However, the mechanisms of the antioxidative and anti-inflammatory effects of pepino leaf in preventing alcoholic fatty liver remain unknown. In this study, Lieber–DeCarli ethanol-containing liquid diet was used to induce alcoholic hepatic injury in C57BL/6 mice. The hepatoprotective effects and the related mechanisms of aqueous extract of pepino leaf (AEPL) were examined. Our results showed that 2% AEPL treatments protected the liver from ethanol-induced injury through reducing serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), total cholesterol (TC) and triglyceride (TG) (all p < 0.05). AEPL had the effects in improving the ethanol-induced lipid accumulation in mice under histological examination. Molecular data indicated that the anti-lipid accumulation effect of AEPL might be mediated via inducing hepatic levels of phospho-adenosine monophosphate-activated kinase (p-AMPK) and peroxisome proliferator-activated receptor (PPAR)-α, and reducing the expressions of hepatic lipogenic enzymes, including sterol regulatory element-binding protein (SREBP)-1c, acetyl-CoA carboxylase (ACC), and fatty acid synthase (FAS) (all p < 0.05). AEPL also decreased hepatic levels of thiobarbituric acid relative substances (TBARS), tumor necrosis factor (TNF)-α, and interleukin (IL)-6, as well as the expression of nuclear factor kappa B (NF-κB) (all p < 0.05). Moreover, AEPL significantly elevated the activities of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx), and glutathione (GSH) content compared to the ethanol-fed group (all p < 0.05). Our present study suggests that AEPL could protect the liver against ethanol-induced oxidative injury and lipid accumulation.
Highlights
IntroductionCalled liver steatosis, is the earliest response to chronic alcohol abuse and is one of the stages of the alcoholic liver disease
Alcoholic fatty liver, called liver steatosis, is the earliest response to chronic alcohol abuse and is one of the stages of the alcoholic liver disease
Long-term alcohol exposure inhibited lipid β oxidation as both Peroxisome proliferator-activated receptors (PPAR)-α and carnitine palmitoyltransferase 1 (CPT-1) activity are disturbed [1]. These findings suggest that PPAR activation is a promising therapeutic strategy in the alcoholic fatty liver
Summary
Called liver steatosis, is the earliest response to chronic alcohol abuse and is one of the stages of the alcoholic liver disease. Alcoholic fatty liver is considered to be a vicious circle due to abnormal lipogenesis and lipid β-oxidation. According to the previous study, long-term alcohol exposure would increase lipogenesis related with. AMP-activated protein kinase (AMPK) activity, sterol regulatory element binding proteins (SREBPs), acetyl-CoA carboxylase (ACC), and fatty acid synthase (FAS) [3]. Peroxisome proliferator-activated receptors (PPAR)-α is a key element of fatty acid catabolism in the liver as PPAR-α regulates many target genes expression including carnitine palmitoyltransferase 1 (CPT-1) [4]. Long-term alcohol exposure inhibited lipid β oxidation as both PPAR-α and CPT-1 activity are disturbed [1]. These findings suggest that PPAR activation is a promising therapeutic strategy in the alcoholic fatty liver
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