Effect of FGF21 on TLR4/p38MAPK Signaling Pathway in Nonalcoholic Fatty Liver Diseases of Rats
10.11969/j.issn.1673-548X.2018.05.032
- VernacularTitle:FGF21对非酒精性脂肪肝大鼠肝细胞TLR4/p38MAPK通路的影响
- Author:
Xingying CHE
1
;
Jiwu HAN
Author Information
1. 150000,哈尔滨医科大学附属第四医院
- Keywords:
Fibroblast growth factor 21;
Non-alcoholic fatty liver;
TLR4/p38MAPK signal pathway
- From:
Journal of Medical Research
2018;47(5):130-135
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effect of FGF21 on MSG-induced nonalcoholic fatty liver diseases of inflammation and TLR4/p38MAPK signal pathway in rats.Methods Newborn SD rats were randomly divided into control group,MSG group and FGF21 group(n =10).Rats of MSG group and FGF21 group were adiministered with solution of MSG 4g/(kg · d) at 2nd,4th,6th,8th and 10th postnataldays.After being fed for thirteen weeks,rats of FGF21 group was intraperitoneal injected with FGF21 1 mg/(kg · d) for a continuous 32 days.Liver pathology of the rats was analyzed by HE staining.The liver weight,aminotrasferases were observed.The expression of IL-6,TNF-α,TLR4,p38MAPK in liver tissue were determined by fluorescence quantitative PCR and Western blot.Results Compared with the control group,liver tissues of the MSG group changed to bullous steatosis and had inflammatory cell infiltration,the liver weighted,serum activities of ALT,AST,ALP were increased (P ＜ 0.01,P ＜ 0.01,P ＜ 0.01,P ＜ 0.01).The expression of IL-6,TNF-α,TLR4,p38MAPK mRNA and protein expression of TLR4,p38MPAK,p-p38MAPK in rats hepatocyte were increased than those in control group (P ＜ 0.01).After reatment with FGF21,the bullous steatosis and inflammatory cell,liver weighted,serum activities of ALT,AST,ALP were signficantly decreased (P ＜ 0.05,P ＜ 0.01,P ＜ 0.01,P ＜ 0.05),and the levels of IL-6,TNF-a,TLR4,p38 MAPK mRNA and protein expression of TLR4,p38-MPAK,p-p38MAPK were reduced than those of MSG group(P ＜0.01).Conculsion The FGF21 may regulate MSG-induced NAFLD of inflammation through TLR4/p38MAPK signaling pathway in rats.
