BACKGROUND Nonalcoholic fatty liver disease (NAFLD) has become the most common liver disease worldwide. Recent studies have shown that the Angptl2 pathway mediated hepatic inflammatory response plays an important role in the progression of nonalcoholic fatty liver disease. Our study investigated the possible molecular mechanisms of berberine (BBR) in the treatment of the liver inflammatory response in the livers of rats with high-fat diet-induced NAFLD via the Angptl2 pathway. RESULTS At the end of 12 weeks, compared with the control group rats, the high-fat- diet group rats showed obvious pathological and biochemical changes. The levels of pro-infalmmatory cytokines (CCL2, TNF-α) were increased, the infiltration of inflammatory cells (CCR2) was elevated, and the hepatic mRNA and protein levels of Angptl2, NF-κB and Foxo1 were increased to different degrees. Nevertheless, following treatment with BBR, liver tissue pathology, biochemical data, and Angptl2 pathway-related genes expression were significantly ameliorated. CONCLUSIONS Our findings demonstrate that BBR might attenuate the liver inflammatory response in the livers of rats with high-fat diet-induced NAFLD through the regulation of the Angptl2 pathway.

中文翻译：

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小ber碱通过Angptl2途径在非酒精性脂肪肝疾病中的抗炎活性。

背景技术非酒精性脂肪肝疾病（NAFLD）已经成为全世界最常见的肝病。最近的研究表明，Angptl2途径介导的肝炎性反应在非酒精性脂肪肝疾病的进展中起着重要作用。我们的研究探讨了小ber碱（BBR）通过Angptl2途径治疗高脂饮食诱导的NAFLD大鼠肝脏炎症反应的可能分子机制。结果在第12周末，高脂饮食组大鼠与对照组相比有明显的病理和生化变化。炎症前细胞因子（CCL2，TNF-α）水平升高，炎性细胞（CCR2）浸润水平升高，Angptl2的肝mRNA和蛋白水平升高，NF-κB和Foxo1均有不同程度的升高。然而，在用BBR治疗后，肝组织病理学，生化数据和Angptl2通路相关基因的表达得到了明显改善。结论我们的研究结果表明，BBR可能通过调节Angptl2途径减轻高脂饮食诱导的NAFLD大鼠肝脏的肝脏炎症反应。