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Ginsenoside 25-OCH3-PPD Promotes Activity of LXRs To Ameliorate P2X7R-Mediated NLRP3 Inflammasome in the Development of Hepatic Fibrosis

Author:
Han, Xin, Song, Jian, Lian, Li-Hua, Yao, You-Li, Shao, Dan-Yang, Fan, Ying, Hou, Li-Shuang, Wang, Ge, Zheng, Shuang, Wu, Yan-Ling, Nan, Ji-Xing
Source:
Journal of agricultural and food chemistry 2018 v.66 no.27 pp. 7023-7035
ISSN:
1520-5118
Subject:
Panax ginseng, alanine transaminase, apoptosis, aspartate transaminase, blood serum, cytokines, dietary supplements, energy drinks, energy metabolism, herbal medicines, histology, inflammasomes, inflammation, liver, liver cirrhosis, mice, receptors
Abstract:
Ginseng is widely used in energy drinks, dietary supplements, and herbal medicines, and its pharmacological actions are related with energy metabolism. As an important modulating energy metabolism pathway, liver X receptors (LXRs) can promote the resolving of hepatic fibrosis and inflammation. The present study aims to evaluate the regulation of 25-OCH₃-PPD, a ginsenoside isolated from Panax ginseng, against hepatic fibrosis and inflammation in thioacetamide (TAA)-stimulated mice by activating the LXRs pathway. 25-OCH₃-PPD decreases serum ALT/AST levels and improves the histological pathology of liver in TAA-induced mice; attenuates transcripts of pro-fibrogenic markers associated with hepatic stellate cell activation; attenuates the levels of pro-Inflammatory cytokines and blocks apoptosis happened in liver; inhibits NLRP3 inflammasome by affecting P2X7R activation; and regulates PI3K/Akt and LKB1/AMPK-SIRT1. 25-OCH₃-PPD also facilitates LX25Rs and FXR activities decreased by TAA stimulation. 25-OCH₃-PPD also decreases α-SMA via regulation of LXRs and P2X7R-NLRP3 in vitro. Our data suggest the possibility that 25-OCH₃-PPD promotes activity of LXRs to ameliorate P2X7R-mediated NLRP3 inflammasome in the development of hepatic fibrosis.
Agid:
6042937