Exogenous hydrogen sulfide protects fatty liver against ischemia-reperfusion injury by regulating endoplasmic reticulum stress-induced autophagy in macrophage through mediating the class A scavenger receptor pathway in rats.

Abstract:

:Fatty liver disease is a disease manifested with excessive alcohol intake and obese. Importantly, hydrogen sulfide (H2 S) has been revealed to participate in the progression of fatty liver; however, the underlying mechanism has not been clearly elucidated yet. In this study, we aimed to investigate the effects of exogenous H2 S on fatty liver ischemia-reperfusion injury (IRI) through mediating class A scavenger receptor (SRA) pathway in rats. By determining endoplasmic reticulum stress (ERS)-related factors, autophagy markers and apoptosis-related factors in liver tissue and liver function, levels of oxidative stress, inflammatory factors, and hepatocyte apoptosis, the effects of H2 S on IRI-induced autophagy, oxidative stress, and inflammation were all examined in rat model of fatty liver IRI. Results from obtained data showed that H2 S decreased the expression of SRA, Grp78, PERK, CHOP, and Caspase-3, and increased that of LC3-II/LC3-I, in addition to alleviating the pathological changes of liver and reducing the levels of ALT, AST, LDH TBARS, and MDA. Moreover, H2 S decreased the levels of oxidative stress, the expression of pro-inflammatory factors including tumor necrosis factor α, interleukin 1, and interleukin 6, and the apoptosis of hepatocytes. Our findings suggested exogenous H2 S could reduce ERS by mediating the SRA pathway and protect liver function by inducing autophagy, and protect against IRI by reducing oxidative stress and inflammation.

journal_name

Cell Biol Int

authors

Ruan Z,Liang M,Deng X,Lai M,Shang L,Su X

doi

10.1002/cbin.11234

subject

Has Abstract

pub_date

2019-09-04 00:00:00

eissn

1065-6995

issn

1095-8355

pub_type

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