Preprint Article Version 1 This version is not peer-reviewed

Ginsenoside Rh2 Ameliorates Lipopolysaccharide Induced Acute Lung Injury by Regulating the TLR4/ PI3K/Akt/mTOR, Raf-1/MEK/ERK and Keap1/Nrf2/HO-1 Signaling Pathways in Mice

Version 1 : Received: 23 July 2018 / Approved: 23 July 2018 / Online: 23 July 2018 (13:05:06 CEST)

A peer-reviewed article of this Preprint also exists.

Hsieh, Y.-H.; Deng, J.-S.; Chang, Y.-S.; Huang, G.-J. Ginsenoside Rh2 Ameliorates Lipopolysaccharide-Induced Acute Lung Injury by Regulating the TLR4/PI3K/Akt/mTOR, Raf-1/MEK/ERK, and Keap1/Nrf2/HO-1 Signaling Pathways in Mice. Nutrients 2018, 10, 1208. Hsieh, Y.-H.; Deng, J.-S.; Chang, Y.-S.; Huang, G.-J. Ginsenoside Rh2 Ameliorates Lipopolysaccharide-Induced Acute Lung Injury by Regulating the TLR4/PI3K/Akt/mTOR, Raf-1/MEK/ERK, and Keap1/Nrf2/HO-1 Signaling Pathways in Mice. Nutrients 2018, 10, 1208.

Journal reference: Nutrients 2018, 10, 1208
DOI: 10.3390/nu10091208

Abstract

The anti-inflammatory effect of ginsenoside Rh2 (GRh2) is one of the most important ginsenosides. The purpose of this study is to identify the anti-inflammatory and antioxidant effects of GRh2 after LPS challenge lung injury animal model. GRh2 reduced LPS-induced NO, TNF-α, IL-1, IL-4, IL-6 and IL-10 productions in lung tissues. GRh2 treatment decreased the histological alterations in the lung tissues and BALF protein content and total cells number also diminished in LPS-induced lung injury mice. Moreover, GRh2 blocked iNOS, COX-2, the phosphorylation of IκB-α, ERK, JNK, p38, Raf-1 and MEK protein expression which is corresponded to the growth of HO-1, Nrf-2, catalase, SOD and GPx expressions in LPS-induce lung injury. An experimental study has suggested that GRh2 has provided with anti-inflammatory effects in vivo, and its potential therapeutic efficacy in major anterior segment lung diseases.

Subject Areas

Ginsenoside Rh2; Lipopolysaccharide; Acute lung injury; MEK; Nrf-2;

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