DTBNP、DTDP促进INS-1细胞葡萄糖刺激胰岛素分泌

摘要

目的:探讨巯基氧化还原试剂对葡萄糖刺激胰岛素分泌(glucose-stimulated insulin secretion,GSIS)影响,进而揭示其调节胰岛素分泌的可能机制.方法:INS-l细胞经传代培养3~4 d后在KRBH液中,37℃培养箱孵育30 min,再用含有不同浓度葡萄糖和巯基氧化还原试剂的KRBH液中培养60 min.然后留取上清液进行胰岛素测定.结果:(1)INS-1细胞在2.5、5、10、15、20 mmol/L葡萄糖浓度范围内胰岛素分泌量逐渐增加,G5、G10、G15组间两两相比均有统计学意义(P<0.05);(2)与G10组相比,G10+DTBNP、G10+DTDP组胰岛素分泌量显著增加(P<0.05),且该效应可以被DTT所消除.(3)DTBNP、DTDP均能增加NIF处理组胰岛素分泌,但其增加幅度低于非NIF处理组(P<0.05);(4)与非DIA组相比,G10+DIA+DTBNP、G10+DIA+DTDP组胰岛素分泌增加幅度显著减低(P<0.05);(5)同G10组比较,G10+DIA+NIF+DTBNP、G10+DIA+NIF+DTDP组胰岛素分泌值增加(P<0.05).结论:本研究显示巯基氧化还原试剂对GSIS产生调节作用.DTDP、DTBNP可能通过对KATP、L型CaV通道及IP3受体活性的调节,促进胰岛素分泌.%Objective To investigate the role of sulfydral redox agent in the modulation of insulin secretion and the potential mechanism. Methods Insulin secretion was evaluated in INS-1 cells after treatment with different concentrations of glucose and sulfydral redox agents by a standard insulin radio immunoassay. Results Glucose concentration-dependently potentiates insulin secretion was observed in INS-1 cells. DTBNP and DTDP could not only significantly increase glucose-stimulated insulin secretion (GSIS), but also increase insulin secretion in nifedipine-pretreated cells, which could be abrogated by DTT. Importantly, pharmacological ablation of L-type calcium channels by nifedipine and/or ablation of K ATP channelby diazoxide both could potentiate glucose-induced insulin secretory. Conclusions Sulfydral redox agent could regulates GSIS. DTBNP and DTDP may increase insulin secretion via regulating the activities of KATP, L-type CaV channel and IP3 receptor.