中文摘要：

目的：探讨抵抗素对HepG2细胞脂质代谢的影响及其与腺苷酸活化蛋白激酶（AMPK）通路的关系。方法：50ng／mL抵抗素及0．5mmol／L的棕榈酸作用HepG2细胞，利用siRNA技术抑制HepG2细胞AMPKα2亚基表达，采用实时荧光定量RT—PCR技术检测脂质代谢相关基因的mRNA水平，用蛋白印迹技术检测AMPK蛋白磷酸化（P—AMPK—Thr172）水平及乙酰辅酶A羧化酶（ACC）蛋白磷酸化（P-ACC-Ser79）水平，尼罗红（NileRed）染色后激光共聚焦显微镜检测胞内脂质含量。结果：在基础及胰岛素刺激条件下，抵抗素增加ACC2mRNA的表达水平及胞内脂质含量（P〈0．05），降低AMPKα2及肝脂肪酶（HL）mRNA的表达、AMPK及ACC磷酸化水平（P〈0．05），对ACC1mRNA表达无影响（P〉0．05）。结论：抵抗素可通过AMPK途径影响脂质代谢：脂肪酸合成增加、抑制三酰甘油分解，导致HepG2肝细胞胞内脂质积聚。

英文摘要：

Objective To investigate the effect of rh-resistin on lipid metabolism in HepG2 cells and to elucidate its relation to AMPK pathway. Methods We treated the HepG2 cells with 50 ng/ml rh-resistin and 0.5 mmol/L palmitic acid, used siRNA technique to inhibite α2 subunite expression of AMPK in HepG2 cells and quantitative RT-PCR to detect ACC1, ACC2, and HL mRNA expression levels of related lipid metabolism genes. The P-AMPK-Thr172 of AMPK and P-ACC-Ser79 of ACC were determined by Western blotting. The Lipid accumu- lation in cells was determined by images of Laser Scanning Confocal Microscope after Nile red staining. Results Rh-resistin decreased the AMPKα2, HL mRNA expressions and the phosphorylation level of AMPK and ACC in both basal and insulin-stimulated conditions （P 〈 0.05） , had no influence on ACC2 mRNA expressions （P 〉 0.05） , while it increased ACC2 mRNA expressions and cytoplasmic lipid droplets in the same conditions （P 〈 0.05）. Conclusion Rh-resistin may affect lipid metabolism via AMPK pathway with increase of fatty acid synthesis and inhibition of triglyceride catabolism, which leading to lipid accumulation in HepG2 cells.