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.
ABSTRACT
0bjective 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 ceils 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 J(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 1ipid 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 thera-peutic target of NAFLD.