Preliminary study on the protective effect of glycosyltransferase Colgalt2 gene deletion on acetaminophen-induced liver injury
10.3760/cma.j.cn501113-20201106-00602
- VernacularTitle:糖基转移酶Colgalt2基因缺失对于对乙酰氨基酚导致的肝损伤的保护作用初探
- Author:
Xiaohui ZHANG
1
;
Lele GUO
;
Hongshan WEI
;
Feng REN
;
Jing ZHANG
Author Information
1. 首都医科大学附属北京佑安医院，北京 100069
- Keywords:
Glycosyltransferase;
Acetaminophen;
Acute liver injury
- From:
Chinese Journal of Hepatology
2021;29(1):67-71
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the protective effect of Colgalt2 gene deletion on acute liver injury induced by acetaminophen (APAP) in mice.Methods:Colgalt2 +/+ wild-type control mice and Colgalt2 -/- mice (all C57BL/6J strains) were selected as the research subject. APAP solution was injected intraperitoneally to establish a mouse model of acute liver injury. The mouse were divided into four groups: Colgalt2 +/+ wild-type control group, Colgalt2 +/+ wild-type drug group (APAP 500 mg/kg), Colgalt2 -/- control group, and Colgalt2 -/- drug group (APAP 500 mg/kg). The survival rate was measured to plot survival curve. Liver function was evaluated by detecting serum ALT and AST levels. Liver histopathological changes were observed by HE staining to evaluate the condition of liver injury. Western blot was used to detect protein c-Jun N-terminal kinase (JNK)-related liver injury. Results:Compared with Colgalt2 +/+ mice, the survival rate was significantly increased after giving APAP to Colgalt2 -/- mice (86.7% vs. 40%), and liver cell necrosis and inflammatory cell infiltrates of Colgalt2 +/+ mice were milder. Serum ALT, and AST level was significantly decreased [ALT: (5 291.9 ± 1 016.34) U/L vs. (1 616.9 ± 330.65) U/L, P = 0.000; AST: (4 978.0 ± 1 028.43) U/L vs. (1 851.0 ± 437.55) U/L, P = 0.000]. The expression level of JNK was significantly decreased in liver tissue. Conclusion:Colgalt2 gene deletion has a protective effect on acute liver injury induced by acetaminophen (APAP) in mice. Therefore, Colgalt2 may be a potential therapeutic option for acetaminophen-induced hepatotoxicity.
