OBJECTIVE: To investigate the role and molecular mechanism of resistin in inflammation of hepatocytes in nonalcoholic steatohepatitis. METHODS: Rat models of NASH were established successfully. The expression of resistin mRNA and protein were examined by quantitative RT-PCR and immunohistolostaining, respectively. The murine hepatocytes AML-12 were incubated with recombinant resistin or LPS for 48 hours, and the concentration of TNF alpha, IL-6 in supernatant of AML-12 cells were quantified by enzyme linked immunosorbent assay (ELISA), the nuclear translocation NF- kappa B were observed by immunofluorescence. RESULTS: The steatosis of hepatocytes, inflammation in the lobule and perisinusoidal fibrosis in livers were found, and the expression of resistin mRNA and protein were increased in livers of rat model of NASH. The expression of resistin mRNA was 2.5 and 4 time higher in 12 weeks and 16 weeks of rat models respectively than that in normal control. The positive staining of resistin protein can be found mainly around the central veins. The concentration of TNF alpha and IL-6 were (1.856 +/- 0.049) pg/ml and (9.463 +/- 1.216) pg/ml in supernantant of AML-12 cells 48 hours after recombinant resistin treatment, and (1.791 +/- 0.046) pg/ml, (8.738 +/- 1.101) pg/ml 48 hours after LPS treatment. There was no significant difference between them, but both were higher than that in normal control (P < 0.01). The NF- kappa B p65 nuclear translocation had been observed in AML-12 cells 3 hours after resistin or LPS treatment. CONCLUSIONS: Resistin can induce the production of TNF alpha, IL-6 and other inflammatory factors by hepatocytes, and therefore is an important inflammatory factor in NASH.
OBJECTIVE: To investigate the role and molecular mechanism of resistin in inflammation of hepatocytes in nonalcoholic steatohepatitis. METHODS:Rat models of NASH were established successfully. The expression of resistin mRNA and protein were examined by quantitative RT-PCR and immunohistolostaining, respectively. The murine hepatocytes AML-12 were incubated with recombinant resistin or LPS for 48 hours, and the concentration of TNF alpha, IL-6 in supernatant of AML-12 cells were quantified by enzyme linked immunosorbent assay (ELISA), the nuclear translocation NF- kappa B were observed by immunofluorescence. RESULTS: The steatosis of hepatocytes, inflammation in the lobule and perisinusoidal fibrosis in livers were found, and the expression of resistin mRNA and protein were increased in livers of rat model of NASH. The expression of resistin mRNA was 2.5 and 4 time higher in 12 weeks and 16 weeks of rat models respectively than that in normal control. The positive staining of resistin protein can be found mainly around the central veins. The concentration of TNF alpha and IL-6 were (1.856 +/- 0.049) pg/ml and (9.463 +/- 1.216) pg/ml in supernantant of AML-12 cells 48 hours after recombinant resistin treatment, and (1.791 +/- 0.046) pg/ml, (8.738 +/- 1.101) pg/ml 48 hours after LPS treatment. There was no significant difference between them, but both were higher than that in normal control (P < 0.01). The NF- kappa Bp65 nuclear translocation had been observed in AML-12 cells 3 hours after resistin or LPS treatment. CONCLUSIONS:Resistin can induce the production of TNF alpha, IL-6 and other inflammatory factors by hepatocytes, and therefore is an important inflammatory factor in NASH.