Exp Clin Endocrinol Diabetes 2020; 128(03): 137-143
DOI: 10.1055/a-0999-0149
Article
© Georg Thieme Verlag KG Stuttgart · New York

Exogenous Hydrogen Sulfide Alleviates-Induced Intracellular Inflammation in HepG2 Cells

Ya-Di Wang
1   Department of Metabolism and Endocrinology, the First Affiliated Hospital of University of South China, Hengyang, China
,
Jiao-Yang Li
1   Department of Metabolism and Endocrinology, the First Affiliated Hospital of University of South China, Hengyang, China
,
Yu Qin
1   Department of Metabolism and Endocrinology, the First Affiliated Hospital of University of South China, Hengyang, China
,
Qiong Liu
1   Department of Metabolism and Endocrinology, the First Affiliated Hospital of University of South China, Hengyang, China
,
Zhe-Zhen Liao
1   Department of Metabolism and Endocrinology, the First Affiliated Hospital of University of South China, Hengyang, China
,
Xin-Hua Xiao
1   Department of Metabolism and Endocrinology, the First Affiliated Hospital of University of South China, Hengyang, China
› Author Affiliations

This work was supported by research grant from the National Natural Science Foundation of China (81270925), Major Scientific Research Projects of Hunan health and family planning commission (A2017011).
Further Information

Publication History

received 11 September 2018
revised 05 August 2019

accepted 01 July 2019

Publication Date:
17 October 2019 (online)

Preview

Abstract

Fatty acids induced hepatic inflammation plays an important role in nonalcoholic fatty liver disease (NAFLD) pathogenesis. Hydrogen sulfide (H2S), an endogenous gasotransmitter, has been established to possess potent anti-inflammation in various human organs. However, the anti-inflammation property of H2S in the fatty liver is still needed to further elucidate. Hence, this study aimed to investigate whether exogenous H2S can protect hepatocytes against inflammation induced by palmitic acid (PA). HepG2 hepatocytes were exposed to PA for 24 h to induce free fatty acids-induced inflammation. The cells were pretreated with NaHS (a donor of H2S) before exposure to PA. Cell viability, inflammatory cytokines (TNF-α, IL-6 and IL-1β), NLRP3 inflammasome and NF-κB were measured by a combination of MTT assay, ELISA, Western blot and Immunofluorescence. Here, we found that exogenous H2S dose-dependently inhibited the expression of pro-inflammatory cytokines, NLRP3 inflammasome and activation of NF-κB signaling in PA-induced HepG2 cells. Thus, H2S might be a candidate therapeutic agent against NAFLD.

Supplementary Material