目的：研究大黄素、小檗碱对HepG2细胞产生胰岛素抵抗的预防作用及机制。方法：首先用MTT法筛选大黄素、小檗碱作用于HepG2细胞的实验浓度，然后用软脂酸诱导HepG2细胞，同时分别加入大黄素、小檗碱干预，并设正常组、对照组进行比较，通过葡萄糖氧化酶法、蒽酮法、RT-PCR法，观察大黄素、小檗碱对HepG2细胞上糖代谢及瘦素长型受体、短型受体mRNA表达水平的影响。结果：对照组成为具有胰岛素抵抗的HepG2细胞，且细胞上瘦素长型及短型受体mRNA的表达水平较正常组显著下降（P < 0.01）；而大黄素、小檗碱组培养液中葡萄糖含量、细胞内糖原含量以及细胞上瘦素长型及短型受体mRNA的表达水平较正常组无明显改变（P > 0.05）。结论：大黄素、小檗碱均能预防HepG2细胞产生胰岛素抵抗，这一作用与它们影响 HepG2细胞上糖代谢及瘦素受体mRNA表达水平有关。

This work aimed to study the prevention effect of emodin and berberine on insulin resistance in HepG2 cells as well as its mechanism. The experimental concentrations of emodin and berberine for HepG2 cells were screened by the MTT assay. The HepG2 cells were induced by free fatty acid, meanwhile emodin and berberine were separately added for intervention. A normal group and a control group were established for comparison. The glucose oxidase method, the anthrone method, the RT-PCR method were adopted to observe the effect of emodin and berberine on on the medium glucose, cell glycogen level, and mRNA expression of long and short leptin receptors in HepG2 cells. For the control group, HepG2 cells became insulin-resistant, and the mRNA expressions of long and short leptin receptors were significantly decreased（P > 0.05）. While for the experimental group, the medium glucose, cell glycogen level and the mRNA expressions of long and short leptin receptors showed no significant change compared with the normal group（P > 0.05）. The results show that both emodin and berberine may prevent FFA in HepG2 cells from inducing insulin resistance, which is probably associated with the effect of emodin and berberine on the medium glucose, cell glycogen level and mRNA expressions of long and short eptin receptors in HepG2 cells.