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目的观察小檗碱对3T3-L1脂肪细胞内脂素(visfatin)表达的影响和探讨小檗碱改善胰岛素抵抗的机制。方法采用RT-PCR法检测不同浓度小檗碱和不同作用时间后,3T3-L1脂肪细胞内脂素mRNA的表达,并以Western印迹方法检测其蛋白水平的表达。结果0～10μmol/L小檗碱剂量依赖性地增加内脂素mRNA的表达,其中10μmol/L时最明显,是空白对照组的4.96倍,其后随着小檗碱浓度的进一步增加,内脂素mRNA的表达反而降低;10μmol/L的小檗碱作用3 h后内脂素mRNA的表达开始明显增强,至作用12 h时表达增强最明显,是基础组的4.57倍,随着作用时间的延长内脂素mRNA的表达虽然有所下降,但到48 h时内脂素mRNA的表达仍比空白对照组明显增高;5、10、20μmol/L的小檗碱均可使内脂素蛋白的表达增加1.13、2.46、2.34倍,与空白对照组相比差异有统计学意义(P<0.05或P<0.01)。结论在一定浓度范围内小檗碱可剂量和时间依赖性地促进离体脂肪细胞内脂素mRNA及蛋白表达。小檗碱对内脂素表达的调节作用可能是其改善机体胰岛素抵抗、降低血糖的机制之一。
Objective To observe the effect of berberine on the expression of visfatin in 3T3-L1 adipocytes and to explore the mechanism of berberine in improving insulin resistance. Methods RT-PCR was used to detect the expression of visfatin mRNA in 3T3-L1 adipocytes after different concentrations of berberine and different time. The expression of visfatin was detected by Western blot. Results 0-10 μmol/L berberine increased the expression of visfatin mRNA in a dose-dependent manner, which was the most obvious at 10 μmol/L, which was 4.96 times that of the blank control group. Later, with the further increase of berberine concentration, The expression of lipoprotein mRNA decreased but the expression of visfatin mRNA increased significantly after 3 h of berberine treatment with 10 μmol/L, and the expression of visfatin began to increase at 12 h, which was 4.57 times that of the basic group. Although the expression of visfatin mRNA was decreased, the expression of visfatin mRNA was still significantly higher than that of the blank control group at 48 h; berberine at 5, 10, and 20 μmol/L could make visfatin protein. The expression increased 1.13, 2.46, and 2.34 times, and there was a significant difference compared with the blank control group (P<0.05 or P<0.01). Conclusion Berberine can promote the expression of visfatin mRNA and protein in isolated adipocytes in a dose-dependent and time-dependent manner. The regulation of visfatin by berberine may be one of the mechanisms for improving body insulin resistance and lowering blood glucose.