Luteolin improves non-alcoholic fatty liver disease in db/db mice by inhibition of liver X receptor activation to down-regulate expression of sterol regulatory element binding protein 1c

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• 作者：Ye Yin^b ; ¹ ; Lu Gao^b ; ¹ ; Haiyan Lin^b ; Yue Wu^b ; Xiao Han^b ; Yunxia Zhu^b ; ^{zhuyx@njmu.edu.cn} ; Jie Li^a ; ^{lijiemd@163.com}
• 关键词：Non-alcoholic fatty liver disease ; Luteolin ; Liver X receptor ; Fatty acid ; db/db mouse
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2017
• 出版时间：22 January 2017
• 年：2017
• 卷：482
• 期：4
• 页码：720-726
• 全文大小：2206 K
• 卷排序：482

文摘

In this study, we report that daily administration of luteolin for 8 weeks improved hepatic steatosis by repressing hepatic TG accumulation and increasing glycogen storage. Luteolin inhibited hepatic de novo lipid synthesis by regulating the LXR-SREBP-1c signaling pathway, which is over-activated in the livers of db/db mice. Further in vitro studies revealed that luteolin can competitively bind to the ligand binding domain to suppress the LXR activation induced by an LXR agonist and high glucose, thereby decreasing TG accumulation in HepG2 cells and primary hepatocytes. Taken together, our results indicate that luteolin can abolish lipid accumulation induced by LXR-SREBP-1c activation both in vivo and in vitro, and may have potential as a therapeutic agent for treating NAFLD.