Oxymatrine attenuates hepatic steatosis in non-alcoholic fatty liver disease rats fed with high fructose diet through inhibition of sterol regulatory element binding transcription factor 1 (Srebf1) and activation of peroxisome proliferator activated receptor alpha (Pparα)

Jun 25, 2013European journal of pharmacology

Oxymatrine reduces liver fat in rats with diet-induced fatty liver by blocking fat-making signals and boosting fat-burning signals

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Abstract

Oxymatrine treatment reduced liver triglyceride levels and body weight gain in non-alcoholic fatty liver disease (NAFLD) rats in a dose-dependent manner.

Treatment with oxymatrine at doses of 40, 80, and 160 mg/kg decreased liver weight and liver index in NAFLD rats.
Oxymatrine decreased serum and liver lipid levels, indicating an improvement in lipid metabolism.
Histopathological analysis confirmed a reduction in liver lipid accumulation following oxymatrine treatment.
The enzymatic activity of fatty acid synthase (FAS) was reduced, while carnitine palmitoyltransferase 1A (CPT1A) activity increased with treatment.
Oxymatrine altered gene expression related to lipid metabolism, down-regulating Srebf1, Fasn, and Acc, while up-regulating Pparα, Cpt1a, and Acox1.

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The aim of this study was to examine the therapeutic effect of oxymatrine, a monomer isolated from the medicinal plant Sophora flavescens Ait, on the hepatic lipid metabolism in non-alcoholic fatty liver (NAFLD) rats and to explore the potential mechanism. Rats were fed with high fructose diet for 8 weeks to establish the NAFLD model, then were given oxymatrine treatment (40, 80, and 160 mg/kg, respectively) for another 8 weeks. Body weight gain, liver index, serum and liver lipids, and histopathological evaluation were measured. Enzymatic activity and gene expression of the key enzymes involved in the lipogenesis and fatty acid oxidation were assayed. The results showed that oxymatrine treatment reduced body weight gain, liver weight, liver index, dyslipidemia, and liver triglyceride level in a dose dependant manner. Importantly, the histopathological examination of liver confirmed that oxymatrine could decrease the liver lipid accumulation. The treatment also decreased the fatty acid synthase (FAS) enzymatic activity and increased the carnitine palmitoyltransferase 1A (CPT1A) enzymatic activity. Besides, oxymatrine treatment decreased the mRNA expression of sterol regulatory element binding transcription factor 1(Srebf1), fatty acid synthase (Fasn), and acetyl CoA carboxylase (Acc), and increased the mRNA expression of peroxisome proliferator activated receptor alpha (Pparα), carnitine palmitoyltransferase 1A (Cpt1a), and acyl CoA oxidase (Acox1) in high fructose diet induced NAFLD rats. These results suggested that the therapeutic effect of oxymatrine on the hepatic steatosis in high fructose diet induced fatty liver rats is partly due to down-regulating Srebf1 and up-regulating Pparα mediated metabolic pathways simultaneously.

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Oxymatrine attenuates hepatic steatosis in non-alcoholic fatty liver disease rats fed with high fructose diet through inhibition of sterol regulatory element binding transcription factor 1 (Srebf1) and activation of peroxisome proliferator activated receptor alpha (Pparα)

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