Effects and mechanism of TREM-1 on inflammatory response and lipid metabolism in mice with nonalcoholic fatty liver disease
10.3760/cma.j.issn.1007-8118.2019.12.013
- VernacularTitle: 髓样细胞触发性受体1对非酒精性脂肪肝小鼠炎症反应和脂质的影响及其机制
- Author:
Jingsong HUANG
1
;
Shenzong RAO
2
;
Jijun HU
3
;
Changgang XIANG
2
;
Min ZHANG
2
;
Xueliang LU
2
;
Haoran SUN
2
;
Jian LI
2
Author Information
1. Department of Transfusion, Xiang'an Hospital of Xiamen University, Xiamen 361101, China
2. Department of Transfusion, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China
3. Department of Transfusion, Wuhan Third Hospital, Wuhan 430000, China
- Publication Type:Journal Article
- Keywords:
Inflammation;
Nonalcoholic fatty liver disease;
Triggering receptor-1 expressed on myeloid cells;
Lipid accumulation
- From:
Chinese Journal of Hepatobiliary Surgery
2019;25(12):937-941
- CountryChina
- Language:Chinese
-
Abstract:
Objective:Analysis of the effect of triggering receptor-1 expressed on myeloid cells (TREM-1) in nonalcoholic fatty liver disease (NAFLD) and the mechanism.
Methods:The oleic acid-treated HepG2 cells were divided into model group, overexpression group, interference group A, interference group B and negative control group. The mouse model of NAFLD was generated and randomly divided into (nuclear factor-κB) NF-κB inhibition group, protein kinase B (AKT) inhibition group, knockout group A, knockout group B and control group. The expression of inflammatory factors and TREM-1 in liver tissue was detected by PCR, and fat accumulation was detected by oil red O staining. Western blotting was used to detect the expression of TREM-1 and signaling pathway proteins, and HE staining was used to detect liver tissue changes.
Results:TREM-1 was up-regulated in liver tissue of NAFLD mice [(0.936±0.127) vs. (0.432±0.105)] and in oleic acid-treated HepG2 cells. In oleic acid-treated HepG2 cells, overexpression of TREM-1 increased inflammatory factor expression and increased lipid droplets; inhibition of TREM-1 expression decreased inflammatory factor expression, and lipid droplets decreased. Knockout of TREM-1 and inhibition of NF-κB in NAFLD mice reduced hepatocyte inflammatory factor expression and reduced liver damage; knockout of TREM-1 and inhibition of AKT reduced liver tissue lipids and drops accumulate.
Conclusions:The overexpression of TREM-1 in NAFLD mice liver tissue can regulate inflammatory factor expression and lipid droplets through NF-κB and AKT signal pathway. TREM-1 might be a potential therapeutic target of NAFLD.
