Hepatoprotective Mechanism of Ginsenoside Rg1 against Alcoholic Liver Damage Based on Gut Microbiota and Network Pharmacology

Author:

Xia Ting1,Fang Bin1,Kang Chaoyan1,Zhao Yuxuan1,Qiang Xiao1,Zhang Xiaodong1,Wang Yiming1,Zhong Tian2,Xiao Jianbo34ORCID,Wang Min1ORCID

Affiliation:

1. State Key Laboratory of Food Nutrition and Safety, Key Laboratory of Industrial Fermentation Microbiology, College of Biotechnology, Tianjin University of Science and Technology, Tianjin 300457, China

2. Faculty of Medicine, Macau University of Science and Technology, Taipa, Macau 999078, China

3. Universidade de Vigo, Department of Analytical and Food Chemistry, Faculty of Sciences, 32004 Ourense, Spain

4. International Research Center for Food Nutrition and Safety, Jiangsu University, Zhenjiang 212013, China

Abstract

Alcoholic liver disease (ALD) is a major public health problem worldwide, which needs to be effective prevention. Ginsenoside Rg1 (GRg1), a bioactive ingredient extracted from ginseng, has benefit effects on health. In this study, 11 potential targets of GRg1 against ALD were firstly obtained by network pharmacology. KEGG pathway enrichment showed that GRg1-target-ALD was closely related to Toll-like receptor (TLR) and nuclear factor-kappa B (NF-κB) signaling pathways. In addition, GRg1 decreased antioxidant levels and increased oxidative levels in alcohol-treated mice, which alleviated oxidative stress-induced hepatic damage. GRg1 enhanced intestinal barrier function via upregulating the levels of tight junction protein and immunoglobulin A. GRg1 also reduced alcohol-induced inflammation by suppressing TLR4/NF-κB pathway, which was consistent with the prediction of network targets. Moreover, GRg1 altered GM population, and Verrucomicrobia, Bacteroidetes, Akkermansia, Bacteroides, Lachnospiraceae_NK4A136_group, and Alloprevotella played positive association with intestinal barrier indicators and negative correlation with hepatic inflammation biomarkers. The results suggest that GRg1 administration might be a promising strategy for protection of alcohol-induced liver damage.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

Cell Biology,Aging,General Medicine,Biochemistry

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