| 不同胰岛素促泌剂对胰岛β细胞凋亡的影响 |
| 投稿时间：2009-08-24 修订日期：2009-12-28 点此下载全文 |
| 引用本文：王庆美,季虹,荣海钦,孙海玲,黄丽芳.不同胰岛素促泌剂对胰岛β细胞凋亡的影响[J].医学研究杂志,2010,39(3):97-101 |
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| 中文摘要:摘要目的研究胰岛素促泌剂在大鼠胰岛素瘤细胞INS-1凋亡中的作用。方法细胞采用大鼠胰岛素瘤细胞株INS-1，实验分5组：A组：格列苯脲（根据药物浓度分3个亚组A1:10μmol/L、A2：1μmol/L、A3：0.1μmol/L）；B组：格列美脲(3个亚组B1:10μmol/L、B2：1μmol/L、B3：0.1μmol/L）；C组：瑞格列奈(3个亚组C1:1μmol/L、C2：0.1μmol/L、C3：0.01μmol/L）；D:阴性对照组（加等量培养基）；E:空白对照组（加等量最高浓度药物溶剂）。各组药物分别干预4h、24h、96h后，观察细胞形态学变化，MTT法检测细胞增生情况，琼脂糖凝胶电泳检测DNA Ladder凋亡条带、TUNEL分析细胞凋亡率，收集细胞培养上清液测定基础和高糖刺激后胰岛素分泌量。结果与阴性对照组相比，空白对照组对细胞凋亡无影响（P>0.05），药物干预4h，格列本脲（A3、A2、A1）、格列美脲（B2、B1）分别使细胞凋亡率增加了2.21、2.5、2.71、2、2.57倍（P<0.05），格列美脲（B3）及瑞格列奈对细胞凋亡率无影响（P>0.05）；药物干预24h，格列本脲（A3、A2、A1）、格列美脲（B3、B2、B1）、瑞格列奈（C2、C1）分别使细胞凋亡率增加了2.35、2.71、2.94、1.71、1.88、2.35、1.53、1.94倍（P<0.05），瑞格列奈（C3）对细胞凋亡率无影响（P>0.05）；药物干预4天，格列本脲（A3、A2、A1）、格列美脲（B3、B2、B1）、瑞格列奈（C3、C2、C1）分别使细胞凋亡率增加3.7、4.5、8.35、3.2、3.8、7、2.8、3.6、4.5倍（P<0.05）。组间比较差异有统计学意义（P<0.05）。结论胰岛素促泌剂可以引起胰岛β细胞的凋亡，且其促凋亡的作用呈时间-剂量依赖性增加，说明胰岛素促泌剂在胰岛β细胞凋亡中的作用，可为胰岛β细胞凋亡的机制提供依据，指导2型糖尿病患者合理用药。 |
| 中文关键词:胰岛素促泌剂 INS-1细胞 凋亡 |
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| The Effect of Insulin Secretagogues on Apoptosis of Pancreatic Beta Cells INS-1 |
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| Abstract:AbstractObjectiveTo study the possible effect of insulin secretagogues on apoptosis in cells of INS-1 cell lines,which is a rat pancreatic beta-cell line derived from the original radiation induced tumor. MethodsINS-1 cell line was routinely cultured and devided into five groups:A: Glibenclamide group;B: Glimepiride group;C: Repaglinide group;D: negative control group;E: positive control group. MTT method was employed to evaluate the proliferation of the INS-1 cell line. Moreover, DNA Ladder and TUNEL method were enrolled to analyze the apoptosis of the INS-1 cell line.Radioimmunoassay ( RIA) was used to investigate the insulin secretion. ResultsIncubating INS-1 with insulin secretagogues showed obvious apoptosis as compared with control group(P<0.05).The INS-1 cell line was treated by different concentrations of different groups for different times. Compared with negtive control group,after treated for 4 hours, cell′s apoptosis in Glibenclamide group(0.1μmol/L,1μmol/L,10μmol/L) was obviously increased by 2.21, 2.5, 2.71 folders(P<0.05), Glimepiride(0.1μmol/L) didn′t increase cells′ apoptosis(P>0.05) ,Glimepiride(1μmol/L,10μmol/L) increased cell′s apoptosis by 2 and 2.57 folders(P<0.05).Repaglinide(0.01μmol/L,0.1μmol/L,1μmol/L) didn′t increase cell′s apoptosis (P>005); after 24 hours, Repaglinide(0.01μmol/L) didn′t increase cell′s apoptosis (P>0.05), Glibenclamide (0.1μmol/L,1μmol/L,10μmol/L) increased cell′s apoptosis by2.35, 2.71, 2.94 folders(P<0.05), Glimepiride (0.1μmol/L,1μmol/L,10 μmol/L) increased cell′s apoptosis by1.71, 1.88, 2.35 folders(P<0.05), Repaglinide (0.1μmol/L,1μmol/L) increased cell′s apoptosis by 153, 1.94 folders(P<0.05); after treated for 96 hours, Glibenclamide (0.1μmol/L,1μmol/L,10μmol/L), Glimepiride (0.1μmol/L,1μmol/L,10μmol/L), Repaglinide(0.01μmol/L, 0.1μmol/L,1μmol/L) increased cell′s apoptosis by 3.7, 4.5, 835, 3.2, 3.8, 7, 2.8, 3.6 and 4.5 folders (P<0.05). ConclusionInsulin secretagogues can increase apoptosis of INS-1 cells in a time- and dose-dependent manner．This provides evidence for the mechanism of pancreatic beta cells′ apoptosis, and also provides a new thought for studying the pancreatic islet cell function and guides reasonable use of insulin secretagogues in type 2 diabetes mellitus. |
| keywords:Insulin secretagogues INS-1 cell Apoptosis |
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