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Abstract Title:

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

Abstract Source:

J Agric Food Chem. 2018 Jul 11 ;66(27):7023-7035. Epub 2018 Jul 2. PMID: 29929367

Abstract Author(s):

Xin Han, Jian Song, Li-Hua Lian, You-Li Yao, Dan-Yang Shao, Ying Fan, Li-Shuang Hou, Ge Wang, Shuang Zheng, Yan-Ling Wu, Ji-Xing Nan

Article Affiliation:

Xin Han

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-OCH-PPD, a ginsenoside isolated from Panax ginseng, against hepatic fibrosis and inflammation in thioacetamide (TAA)-stimulated mice by activating the LXRs pathway. 25-OCH-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-OCH-PPD also facilitates LX25Rs and FXR activities decreased by TAA stimulation. 25-OCH-PPD also decreasesα-SMA via regulation of LXRs and P2X7R-NLRP3 in vitro. Our data suggest the possibility that 25-OCH-PPD promotes activity of LXRs to ameliorate P2X7R-mediated NLRP3 inflammasome in the development of hepatic fibrosis.

Study Type : Animal Study, In Vitro Study

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Sayer Ji
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