Objective:To observe the influence of p38 mitogen-activated protein kinase(P38MAPK)signal transduction pathway on the inflammatory reaction and to explore the role of P38 MAPK in nonalcoholic fatty liver disease(NAFLD). Methods:Totally 36 healthy adult male SD rats were randomly divided into three equal groups:normal control group

high sugar model group and SB203580 pretreatment group. Rats in high sugar model group were administered with high-carbohydrate diet for 12 weeks;rats in SB203580 group was administered with high-carbohydrate diet for 12 weeks and injected via abdominal cavity weekly. At the 12 weeks

rats were sacrificed

and pathological changes of the liver tissue were examined with light microscope. Serum biochemistry

liver index

insulin resistance and inflammatory factor expression levels of liver homogenate were examined. P38 MAPK and phospho-p38MAPK(P-P38MAPK)expression condition were determined by Western blot. Results:Compared with those in normal control group

the obvious hepatic steatosis was observed in high sugar model group and alanine aminotransferase

aspertate aminotransferase

glucose

cholesterol

triglyceride in the serum

liver index

insulin resistance and tumor necrosis factor-α

interleukin-6 of liver homogenate were increased obviously in high sugar model group. Compared with those in high sugar model group

those indexes were improved in SB203580 pretreated group. The expression levels of P-P38 MAPK in liver tissues were significantly higher in high sugar model group than in control group and the expression of p-p38 MAPK were reduced significantly in SB203580-group than in high sugar model group. There was no difference in P38 MAPK expression among three groups. Conclusion:P38MAPK signal transaction path participates in cytokines releasion process and plays an important role in NASH. Inhibition of P38 MAPK activity has the potential as an effective therapeutic strategy in interventions of NAFLD.