脂肪性肝炎
脂肪肝
未折叠蛋白反应
自噬
内科学
内分泌学
甘油三酯
切碎
下调和上调
内质网
化学
细胞凋亡
医学
生物化学
胆固醇
化疗
疾病
基因
作者
Shu Fang Jia,Lianyu Jin,Xiaoyan Cheng,Jingyi Wu,Xiaokun Yao,Jingping Shao,Congcong Zhang,Danwei Cen,Bin Cheng,Jing Wang,Lei Chen,Xiaomin Yao
标识
DOI:10.1080/03639045.2022.2106238
摘要
Background and objective Non-alcoholic fatty liver disease (NAFLD) is a manifestation of the metabolic syndrome in the liver, and non-alcoholic steatohepatitis (NASH) represents its advanced stage. Bicyclol has protective activity against NAFLD in mice; however, the effect of bicyclol on high-fat diet (HFD)-induced NASH and its underlying molecular mechanism remains unknown particularly anti-endoplasmic reticulum (ER) stress and autophagic machinery potentials. Therefore, the present study was performed to investigate the protective effect and underlying mechanisms of bicyclol action on NAFLD/NASH.Methods Mice were fed an HFD to induce NAFLD/NASH, and bicyclol was administered as a treatment. Biochemistry and histopathological assays were performed to evaluate the effects of bicyclol on NAFLD/NASH. Moreover, the levels of hepatic ER stress- and autophagy-related markers were determined by western blotting.Results The present results revealed that bicyclol exerted significant protective effects against HFD-induced NAFLD/NASH. This activity was evidenced by the decrease in elevated serum transaminase and hepatic triglyceride levels, and the attenuation of negative histopathological changes. Bicyclol considerably alleviated hepatic inflammation and apoptosis. The protein expression of ER stress-related markers, including C/EBP homologous protein (CHOP) and glucose-regulated protein 78 (GRP78), was downregulated by the bicyclol treatment in HFD-induced mice. However, the protein expression of autophagy-related markers (LC3 and Beclin 1) was upregulated by the treatment with bicyclol.Conclusion Bicyclol protected HFD-induced NASH, and partly due to its ability of reducing ER stress and promoting autophagy.
科研通智能强力驱动
Strongly Powered by AbleSci AI