【摘 要】
：
目的 研究解毒通络调肝方对大鼠胰岛细胞瘤细胞(islet cell tumor cells,INS-1)糖毒性的保护作用机制.方法 以大鼠胰岛细胞瘤细胞为研究对象,用MTT比色法检测解毒通络调肝方干预后INS-1细胞存活率的情况;不同浓度的解毒通络调肝方干预高糖诱导的INS-1细胞;通过葡萄糖刺激胰岛素分泌(glucose-stimulated insulin secretion test,GSIS)检验胰岛素分泌量;实时逆转录聚合酶链反应法测定INS1、INS2、胰十二指肠同源盒因子1(pancreat
【机 构】
：
130017 长春中医药大学;长春中医药大学附属医院实验中心;广州中医药大学深圳医院(福田)内分泌科
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目的 研究解毒通络调肝方对大鼠胰岛细胞瘤细胞(islet cell tumor cells,INS-1)糖毒性的保护作用机制.方法 以大鼠胰岛细胞瘤细胞为研究对象,用MTT比色法检测解毒通络调肝方干预后INS-1细胞存活率的情况;不同浓度的解毒通络调肝方干预高糖诱导的INS-1细胞;通过葡萄糖刺激胰岛素分泌(glucose-stimulated insulin secretion test,GSIS)检验胰岛素分泌量;实时逆转录聚合酶链反应法测定INS1、INS2、胰十二指肠同源盒因子1(pancreatic and duodenal homeobox 1,PDX1)和MafA的mRNA表达水平;蛋白印迹实验检测INS-1细胞中内质网的跨膜蛋白[阻抗性激酶lα(inositol-requiring enzyme 1α,IRE1α)、双链RNA依赖性蛋白激酶样内质网激酶(protein kinase R-like endoplasmic reticulum kinase,PERK)和活化的转录因子6(activating transcription factor 6,ATF6)]的表达.结果 通过从TCMSP数据库中总结分析解毒通络调肝方中潜在成分,表明该方具有较好的稳定性和重复性;不同浓度的解毒通络调肝方对INS-1细胞活力无抑制作用(P>0.05),但能够抑制高糖诱导的胰岛素分泌的降低(P<0.05),提高INS1、INS2、PDX1和MafA的mRNA表达(P<0.05),抑制IRE1α、PERK、ATF6蛋白表达(P<0.05).结论 解毒通络调肝方能够通过提高胰岛素合成相关基因的表达,促进INS-1细胞的胰岛素分泌,降低内质网应激,以恢复细胞内稳态平衡,减少糖毒性对β细胞损伤.
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