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DTBNP、DTDP促进INS-1细胞葡萄糖刺激胰岛素分泌 被引量:1

DTBNP and DTDP increase glucose-stimulated insulin secretion in INS-1 cell
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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K_ATP、L型Ca_V通道及IP_3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 KATPchannelby 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 K_ATP, L-type Ca_Vchannel and IP_3 receptor.
出处 《实用医学杂志》 CAS 北大核心 2016年第6期883-886,共4页 The Journal of Practical Medicine
基金 江苏省自然科学基金青年项目(编号:BK2015041792) 南京医科大学科技发展基金重点项目(编号:2011NJUM248)
关键词 葡萄糖刺激胰岛素分泌 INS-1细胞 巯基氧化还原试剂 Glucose-stimulated insulin secretion INS-1 cell Sulfydra lredox agents
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