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      Rosuvastatin ameliorates high-fat and high-cholesterol diet-induced nonalcoholic steatohepatitis in rats.

      Liver International
      Acyl-CoA Dehydrogenase, Long-Chain, metabolism, Acyl-CoA Oxidase, Alanine Transaminase, blood, Animals, Azo Compounds, Carnitine O-Palmitoyltransferase, Catalase, Cholesterol, Cholesterol, Dietary, adverse effects, DNA Primers, genetics, Diet, High-Fat, Enzyme-Linked Immunosorbent Assay, Fatty Acids, Nonesterified, Fatty Liver, drug therapy, etiology, Fluorobenzenes, pharmacology, therapeutic use, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Immunohistochemistry, Liver, pathology, Male, Non-alcoholic Fatty Liver Disease, Pyrimidines, Rats, Rats, Sprague-Dawley, Real-Time Polymerase Chain Reaction, Sulfonamides

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          Abstract

          Statins, which are inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase and inhibit endogenous cholesterol synthesis, possess pleiotropic activities, such as anti-inflammatory, anti-oxidative and antifibrotic effects. Here, we investigated whether statins ameliorate steatohepatitis using a high-fat and high-cholesterol (HFHC) diet-induced rat model. Eight-week-old male Sprague-Dawley rats were fed control chow or HFHC diet. Half of the HFHC diet-fed rats were orally administered 2 mg/kg/day rosuvastatin for 12 weeks. Hepatic injury, steatosis, fibrosis and markers of lipid peroxidation/oxidant stress were evaluated. As previously reported, HFHC diet induced steatohepatitis in rat livers with hypercholesterolaemia. Rosuvastatin decreased Oil Red O stained-positive areas, liver/body weight ratio, serum total cholesterol levels and hepatic free fatty acid contents in HFHC diet-fed rats. Further study revealed that rosuvastatin significantly decreased hepatic mRNA expression of tumour necrosis factor-α and interleukin-6, serum alanine aminotransferase levels and hepatic lobular inflammation grade. Hepatic fibrosis was also ameliorated by rosuvastatin with decreases in hepatic mRNA expression of transforming growth factor-β, connective tissue growth factor and type-1 procollagen. Similarly, hepatic Sirius red stained or α-smooth muscle actin stained-positive areas and expression of markers of lipid peroxidation/oxidant stress [hepatic 8-hydroxy-oxyguanosine and hepatic 4-hydroxy-2-nonenal] were decreased. Interestingly, whereas the expression of carnitine palmitoyltransferase-1 and long-chain acyl-CoA dehydrogenase was not affected, that of catalase and acyl-coA oxidase was restored. These data suggest that rosuvastatin improved not only hepatic steatosis but also hepatic injury and fibrosis via improved peroxisomal β-oxidation in this rat HFHC model. © 2012 John Wiley & Sons A/S.

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