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首页> 外文期刊>Journal of biochemical and molecular toxicology >Indomethacin decreases insulin secretion by reducing KCa3.1 as a biomarker of pancreatic tumor and causes apoptotic cell death
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Indomethacin decreases insulin secretion by reducing KCa3.1 as a biomarker of pancreatic tumor and causes apoptotic cell death

机译：吲哚美辛通过将KCA3.1减少作为胰腺肿瘤的生物标志物而降低胰岛素分泌，并导致凋亡细胞死亡

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Insulinomas originate from pancreatic β cells and it is the most widely known tumor. Indomethacin is a nonsteroidal anti-inflammatory drug, which is used for blocking the production of some natural substances that cause inflammation and decrease pain. In this study, I aimed to investigate the effects of indomethacin on rat insulinoma INS-1 cells. The relationship between cell death and insulin metabolism was determined with the administration of indomethacin. The cell viability by WST-1; the apoptosis and necrosis levels by ELISA kits; malondialdehyde levels by spectrophotometer; and beclin, intracellular insulin, insulin secretion, KCa3.1, insulin receptor (IR), glucose transporter type 2 (GLUT2), activating transcription factor 2 (ATF2), Elk1, c-Jun, Akt and phosphorylated ATF2, Elk1, c-Jun, Akt, intracellular betacellulin and betacellulin secretion levels by Western blot analysis investigated. The Ins1, Ins2, IR, GLUT2, ATF2, Elk1, c-Jun, Akt, and Betacellulin gene expression levels were determined by the real-time quantitative reverse transcription-polymerase chain reaction method. Apoptotic cell death was observed with the administration of indomethacin. The insulin secretion and Ins1, Ins2 gene expression levels decreased. The insulin receptor and GLUT2 levels increased, while KCa3.1 (KCNN4) levels decreased with the administration of indomethacin to insulinoma INS-1 cells. A decrease was observed in the total c-Jun, phosphorylated ATF2, Elk1, c-Jun, and Akt levels. Betacellulin secretion levels increased. In insulinoma INS-1 cells, apoptotic cell death occurred in the following manner: (i) indomethacin might decrease insulin secretion by reducing KCa3.1, (ii) might inactivate the JNK/ERK pathway with the inactivity of transcription factors.
机译：胰岛素瘤起源于胰腺β细胞，是最广为人知的肿瘤。吲哚美辛是一种非甾体抗炎药，用于阻止某些引起炎症和减轻疼痛的天然物质的产生。在本研究中，我旨在研究吲哚美辛对大鼠胰岛素瘤INS-1细胞的影响。通过服用消炎痛确定细胞死亡与胰岛素代谢之间的关系。WST-1对细胞活力的影响；ELISA试剂盒检测细胞凋亡和坏死水平；分光光度计测定丙二醛水平；和beclin，细胞内胰岛素，胰岛素分泌，KCa3。1、胰岛素受体（IR）、葡萄糖转运体2型（GLUT2）、激活转录因子2（ATF2）、Elk1、c-Jun、Akt和磷酸化ATF2、Elk1、c-Jun、Akt、细胞内betacellulin和betacellulin分泌水平通过Western blot分析进行调查。通过实时定量逆转录聚合酶链反应法测定Ins1、Ins2、IR、GLUT2、ATF2、Elk1、c-Jun、Akt和β细胞球蛋白基因表达水平。吲哚美辛可导致细胞凋亡。胰岛素分泌和Ins1、Ins2基因表达水平降低。胰岛素受体和GLUT2水平升高，而KCa3水平升高。1（KCNN4）水平随着吲哚美辛对胰岛素瘤INS-1细胞的作用而降低。观察到总c-Jun、磷酸化ATF2、Elk1、c-Jun和Akt水平降低。Betacellin分泌水平增加。在胰岛素瘤INS-1细胞中，凋亡细胞死亡的发生方式如下：（i）吲哚美辛可能通过减少KCa3而减少胰岛素分泌。1，（ii）可能通过转录因子的失活使JNK/ERK途径失活。

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