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目的:胡椒碱和小檗碱分别是温里药荜茇和清热药黄连的主要成分,二者均可以改善胰岛素抵抗。本研究通过建立3T3-L1脂肪细胞胰岛素抵抗模型[1,2],观察胡椒碱和小檗碱对该细胞模型的糖代谢紊乱的干预作用,意在探讨药效相似、药性相反的胡椒碱是否同小檗碱一样可以通过调节腺苷酸活化蛋白激酶AMPK而改善胰岛素抵抗。方法:诱导3T3-L1脂肪细胞分化为成熟的脂肪细胞后,采用1μM地塞米松作用48h建立脂肪细胞胰岛素抵抗模型,以AMPK激活剂AICAR和罗格列酮为阳性药,观察不同浓度的胡椒碱和小檗碱作用该模型48h后对糖代谢紊乱的调节作用,继而采用Western blot检测药物作用不同时间后细胞中AMPKα的水平变化。结果:胡椒碱、小檗碱同阳性药AICAR、罗格列酮一样在作用该脂肪细胞胰岛素抵抗模型48h后均可改善糖代谢紊乱。Western blot检测结果:与模型组比较,40u M胡椒碱、5u M小檗碱同阳性AICAR一样在作用脂肪细胞胰岛素抵抗模型6h,12h和24h后,P-AMPKα的蛋白表达明显提高。结论:胡椒碱同小檗碱一样能够改善糖代谢紊乱,其机理有可能是通过调节AMPK信号通路中的AMPKα的活性而改善胰岛素抵抗的。
PURPOSE: Piperine and berberine are the main constituents of both the warmth-ing medicine and the heat-clearing berberis, both of which can improve insulin resistance. In this study, through the establishment of 3T3-L1 adipocyte insulin resistance model [1,2] observed piperine and berberine intervention in the disorder of glucose metabolism in the cell model intended to explore the similar efficacy and opposite side piperine is Like berberine, insulin resistance can be improved by modulating adenylate-activated protein kinase AMPK. Methods: After induced 3T3-L1 adipocytes to differentiate into mature adipocytes, 1μM dexamethasone was used for 48h to establish adipocyte insulin resistance model. AMPK activators AICAR and rosiglitazone were used as positive drugs to observe the effects of different concentrations of piperine And berberine 48h after the model of glucose metabolism disorder regulation, followed by Western blot detection of drug effect after different periods of time AMPKα levels. Results: Piperine and berberine, as the positive drugs AICAR and rosiglitazone, could improve the disorder of glucose metabolism 48 h after the model of insulin resistance of adipocytes. Western blot results: compared with the model group, 40uM piperine and 5uM berberine, like positive AICAR, significantly increased P-AMPKα protein expression at 6h, 12h and 24h after acting on adipocyte insulin resistance model. CONCLUSION: Piperine can improve glucose metabolism disorder like berberine. Its mechanism may be that it can improve insulin resistance by regulating the activity of AMPKα in AMPK signaling pathway.