Gegen Qinlian Decoction abates nonalcoholic steatohepatitis associated liver injuries via anti-oxidative stress and anti-inflammatory response involved inhibition of toll-like receptor 4 signaling pathways

Biomedicine & Pharmacotherapy

Tong-tong Liu¹  Jun-qing Sheng²  Ying-qian Cao³  Ya-nan Xue³  Chang-hua Zhang³  Qin Xiao³  Min Shi³  Chen Chen³  Zheng cao⁴  Li-fen Zhou⁴  Ke-zhong Deng⁵  Xiao-quan Luo⁶ 

[1] Corresponding author at: College of Life Science, Nanchang University, No. 999 University Avenue, Nanchang, Jiangxi, 330031, PR China.;College of Life Science, Nanchang University, Nanchang, 330031, PR China;College of Pharmacy, Jiangxi University of Traditional Chinese Medicine, Nanchang, Jiangxi, 330004, PR China;College of Traditional Chinese Medicine, Jiangxi University of Traditional Chinese Medicine, Nanchang, Jiangxi, 330004, PR China;Experimental Animal Science and Technology Center of TCM, Jiangxi University of Traditional Chinese Medicine, Nanchang, Jiangxi 330004, PR China;Large Precise Instruments Shared Services Center of TCM, Jiangxi University of Traditional Chinese Medicine, Nanchang, Jiangxi, 330004, PR China;

关键词: Gegen Qinlian Decoction;    Non-alcoholic steatohepatitis;    Inflammation;    Oxidative stress;    Hepatic lipid metabolism;   

DOI  :  

来源: DOAJ

【 摘 要 】

Gegen Qilian Decoction (GGQLD) is a well-established classic Chinese medicine prescription in treating nonalcoholic steatohepatitis (NASH). However, the molecular mechanism of GGQLD action on NASH is still not clear. This study aimed to assess the anti-NASH effect of GGQLD, and to explore its molecular mechanisms in vivo and in vitro. In HFD-fed rats, GGQLD decreased significantly serum triglyceride (TG), cholesterol (CHO), total bile acid (TBA), low-density lipoprotein (LDL), free fatty acid (FFA) and lipopolysaccharide (LPS) levels, increased levels of differentially expressed proteins (DEPs) Ahcy, Gpx1, Mat1a, GNMT, and reduced the expression of ALDOB. In RAW264.7 macrophages, GGQLD reduced the expression levels of inflammatory factors TNF-α and IL-6 mRNA, and diminished NASH by increasing differentially expressed genes (DEGs) CBS, Mat1a, Hnf4α and Pparα to reduce oxidative stress or lipid metabolism. The results of DEGs verification also showed that GGQLD up-regulated expressions of Hnf4α, Pparα and Cbs genes. In HepG2 cells, GGQLD decreased IL-6 levels and intracellular TG content, and inhibited FFA-induced expression of toll-like receptor 4 (TLR4). In summary, GGQLD abates NASH associated liver injuries via anti-oxidative stress and anti-inflammatory response involved inhibition of TLR4 signal pathways. These findings provide new insights into the anti-NASH therapy by GGQLD.

【 授权许可】

Unknown