Dexmedetomidine alleviates LPS/D-Gal-induced acute liver injury via up-regulation of LC3-II expression in mice.
- Author:
Xiao-Jiao HE
1
;
Bin XIE
2
;
Song HUANG
3
;
Ming-Hua LIU
2
Author Information
1. Department of Pharmacy, Chongqing Armed Corps Police Hospital, Chongqing 400061, China.
2. Center of Emergency and Trauma, First Affiliated Hospital of Army Medical University, Chongqing 400038, China.
3. Center of Emergency and Trauma, First Affiliated Hospital of Army Medical University, Chongqing 400038, China. huangsong@cqmu.edu.cn.
- Publication Type:Journal Article
- MeSH:
Alanine Transaminase;
Animals;
Chemical and Drug Induced Liver Injury/drug therapy*;
Dexmedetomidine/pharmacology*;
Galactosamine/toxicity*;
Interleukin-6/blood*;
Lipopolysaccharides/toxicity*;
Liver;
Male;
Mice;
Mice, Inbred BALB C;
Microtubule-Associated Proteins/metabolism*;
Tumor Necrosis Factor-alpha/blood*;
Up-Regulation
- From:
Acta Physiologica Sinica
2021;73(6):901-908
- CountryChina
- Language:Chinese
-
Abstract:
The aim of the present study was to investigate the effects of dexmedetomidine (DEX) on acute liver injury induced by lipopolysaccharide (LPS)/D-galactosamine (D-Gal) and the underlying mechanism. Male BALB/c mice were intraperitoneally injected with LPS/D-Gal to induce acute liver injury model, and pretreated with DEX or in combination with the autophagy inhibitor, 3-methyladenine (3-MA) 30 min before injection. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity, as well as myeloperoxidase (MPO) activity in liver tissue were determined with the corresponding kits. Serum tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) levels were determined by ELISA. The protein expression levels of LC3-II and P62 in liver tissue were determined by Western blot. Liver histopathological changes were detected by HE staining. The results showed that, compared with control group, LPS/D-Gal enhanced ALT and AST activity, increased TNF-α and IL-6 levels, as well as MPO activity, up-regulated LC3-II and P62 protein expression levels, and significantly induced pathological damage in liver tissue. DEX reversed the above changes in the LPS/D-Gal group, whereas these protective effects of DEX were blocked by 3-MA. The above results suggest that DEX alleviates LPS/D-Gal-induced acute liver injury, which may be associated with the up-regulation of LC3-II protein expression and the activation of autophagy.
