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Abstract Title:

Anti-inflammatory effects of ginsenoside Rg1 and its metabolites ginsenoside Rh1 and 20(S)-protopanaxatriol in mice with TNBS-induced colitis.

Abstract Source:

Eur J Pharmacol. 2015 Sep 5 ;762:333-43. Epub 2015 Jun 6. PMID: 26054809

Abstract Author(s):

Sang-Yun Lee, Jin-Ju Jeong, Su-Hyeon Eun, Dong-Hyun Kim

Article Affiliation:

Sang-Yun Lee

Abstract:

Ginsenoside Rg1, one of the main constituents of Panax ginseng, exhibits anti-inflammatory effect. In a preliminary study, it was observed that ginsenoside Rg1 was metabolized to 20(S)-protopanaxtriol via ginsenosides Rh1 and F1 by gut microbiota. We further investigated the anti-inflammatory effects of ginsenoside Rg1 and its metabolites in vitro and in vivo. Ginsenosides Rg1, Rh1, and 20(S)-protopanaxtriol inhibited the activation of NF-κB activation, phosphorylation of transforming growth factor beta-activated kinase 1 and interleukin (IL)-1 receptor-associated kinase, and expression of tumor necrosis factor-α and IL-1β in lipopolysaccharide (LPS)-stimulated macrophages. They also inhibited the binding of LPS to toll-like receptor 4 on the macrophages. Orally administered ginsenoside Rg1, Rh1, or 20(S)-protopanaxtriol inhibited 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colon shortening, myeloperoxidase activity, and expression of IL-1β, IL-17, and tumor necrosis factor-α in mice with TNBS-induced colitis. Theydid not only inhibit TNBS-induced NF-κB activation, but also restored TNBS-induced Th17/Treg imbalance. They restored IL-10 and Foxp3 expression. Moreover, they inhibited Th17 cell differentiation in vitro. Of these metabolites, in vitro and in vivo anti-inflammatory effect of 20(S)-protopanaxtriolwas the most potent, followed by Rh1. These findings suggest that ginsenoside Rg1 is metabolized to 20(S)-protopanaxtriol via ginsenosides Rh1 and F1 and these metabolites particularly 20(S)-protopanaxtriol, may ameliorate inflammatory disease such as colitis by inhibiting the binding of LPS to TLR4 on macrophages and restoring the Th17/Treg imbalance.

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Sayer Ji
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