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Berberine attenuates hepatic oxidative stress in rats with non-alcoholic fatty liver disease via the Nrf2/ARE signalling pathway

机译:小ber碱通过Nrf2 / ARE信号传导途径减轻非酒精性脂肪肝大鼠的肝氧化应激

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摘要

The present study investigated the effects of berberine (BBR) on hepatic oxidative stress and the nuclear factor erythroid 2-related factor 2/antioxidant response element (Nrf2/ARE) signalling pathway in rats in which non-alcoholic fatty liver disease (NAFLD) was induced by a high-fat diet. Rats were randomly divided into three groups: The normal control (NC), high-fat diet (HFD) and BBR groups. The NC group received a normal diet, while the other two groups were fed a high-fat diet. The rats in the BBR group were also fed BBR (100 mg/kg body weight) daily. A total of 8 weeks later, serum and liver lipid levels were measured. Hepatic histopathological changes were observed with haematoxylin and eosin and Oil Red O staining. Transmission electron microscopy was performed to observe the ultrastructural changes of the liver. The levels of superoxide dismutase (SOD), glutathione (GSH) and malondialdehyde (MDA) in the liver were measured. Quantitative polymerase chain reaction and western blotting were performed to investigate the expression of genes in the Nrf2/ARE signalling pathway in the liver. Histopathological results demonstrated that rats fed a high-fat diet for 8 weeks developed NAFLD, characterized by hepatic steatosis. BBR significantly decreased the body weight and liver weight. BBR markedly reduced hepatic steatosis, and the serum and liver lipid levels. Hepatic SOD and GSH levels were increased, while MDA levels were decreased by BBR co-administered with a high-fat diet. Additionally, the Nrf2/ARE signalling pathway was revealed to be involved in the protective effect of BBR on rats fed a high-fat diet. In conclusion, BBR may alleviate hepatic oxidative stress in rats with NAFLD, which may be partly attributed to the activation of the Nrf2/ARE signalling pathway.
机译:本研究调查了小ber碱(BBR)对非酒精性脂肪肝疾病(NAFLD)所致大鼠肝氧化应激和核因子红系2相关因子2 /抗氧化反应元件(Nrf2 / ARE)信号通路的影响。由高脂饮食诱导。将大鼠随机分为三组:正常对照组(NC),高脂饮食(HFD)和BBR组。 NC组接受正常饮食,而其他两组则接受高脂饮食。 BBR组的大鼠也每天喂BBR(100 mg / kg体重)。总共8周后,测量血清和肝脂质水平。用苏木精和曙红和油红O染色观察肝组织病理学变化。进行透射电子显微镜观察肝脏的超微结构变化。测量肝脏中的超氧化物歧化酶(SOD),谷胱甘肽(GSH)和丙二醛(MDA)的水平。进行了定量聚合酶链反应和蛋白质印迹实验,以研究肝脏Nrf2 / ARE信号通路中基因的表达。组织病理学结果表明,喂食高脂饮食8周的大鼠出现了以肝脂肪变性为特征的NAFLD。 BBR显着降低了体重和肝脏重量。 BBR明显减少了肝脂肪变性以及血清和肝脂质水平。 BBR与高脂饮食合用时,肝脏的SOD和GSH含量升高,而MDA含量降低。此外,Nrf2 / ARE信号通路被揭示与BBR对高脂饮食喂养的大鼠的保护作用有关。总之,BBR可以减轻NAFLD大鼠的肝氧化应激,这可能部分归因于Nrf2 / ARE信号通路的激活。

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