The effect of resistin on nuclear factor-kB and tumor necrosis factor-a expression in hepatic steatosis / 中华肝脏病杂志

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the potential regulatory role played by the hormone resistin in lipid metabolism and expression of nuclear factor (NF)-kB and tumor necrosis factor (TNF)-a during hepatic steatosis.</p><p><b>METHODS</b>A non-alcoholic fatty liver disease (NAFLD) cell model was established by treating the normal human hepatic cell line, L02, with palmitic acid. Four research groups of L02 cells were generated C group (control, no palmitic acid treatment), P group (NAFLD model, treated with 20 microg/ml palmitic acid), CR group (C group treated with 50 microg/L recombinant human resistin), and PR group (P group treated with 50 microg/L recombinant human resistin). All treatments were carried out for 72 hours. Oil red O staining was used to detect the intracellular changes in lipid drops. Biochemical assays were used to measure triglycerides (TGs), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transpeptidase (GGT) levels in culture medium. The mRNA and protein expression levels of insulin receptor substrate (IRS)-2, NF-kB, and TNF-a were determined by reverse transcription-polymerase chain reaction and Western blot analysis, respectively.</p><p><b>RESULTS</b>The TG, ALT, AST, and GGT levels were higher in the P, CR, and PR groups than in the C group. The NF-kB mRNA level was also higher in the P, CR, and PR groups (Student's t = 17.64, 22.03, 26.06 respectively) than in the C group, as was the TNFa mRNA level ( t = 5.67, 5.38, 11.64), but the IRS-2 mRNA level was lower ( t = 8.19, 9.23, 20.93) (all, P less than 0.05). In addition, no significant difference in these mRNA levels were found between the P group and the CR group (NF-kB t = 1.75, TNFa t = 0.58, IRS-2 t = 2.14; all, P more than 0.05). The detected protein levels of NF-kB, TNFa, and IRS-2 were consistent with the mRNA levels.</p><p><b>CONCLUSION</b>Resistin can promote steatosis in LO2 cells through the NF-kB signaling pathway, thereby contributing to the NAFLD pathogenic process.</p>