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| Neu-P11在胰岛素抵抗脂肪细胞模型中对胰岛素受体后信号通路的影响 |
| 李秀平1,蔡世昌2*,尹卫东3,张素君4,卢琼2,李兴2 |
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| (湖南医药学院检验医学院, 怀化 418000;1. 湖南医药学院检验医学院, 怀化 418000;南华大学医学院心血管疾病研究所, 衡阳 412000;南华大学实验动物学部, 衡阳 412000;湖南医药学院基础医学院, 怀化 418000) |
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| 摘要: |
| 目的：研究褪黑素类似物Neu-P11在3T3-L1脂肪细胞产生胰岛素抵抗后对胰岛素受体后信号传导通路蛋白p-IRS-1、PI3K、p-GSK3β的蛋白表达变化，从而更深入的阐明人工合成的褪黑素类似物Neu-P11对胰岛素抵抗的脂肪细胞模型（3T3-L1）中信号通路的影响。方法：采取“鸡尾酒法”培养与分化前脂肪细胞（3T3-L1细胞），建立胰岛素抵抗脂肪细胞模型，用Western-blot检测药物作用前后p-IRS-1、 PI3K、p-GSK3β的蛋白质表达变化。结果：胰岛素抵抗模型组的脂肪细胞中通道蛋白p-IRS-1、 PI3K、 p-GSK3β的表达低于对照组的表达(P < 0.05)。药物Mel、 Neu-P11均能明显增加p-IRS-1、 PI3K、 p-GSK3β蛋白表达量(P < 0.05)。Luzindole能够阻断Mel、 Neu-P11增加p-IRS-1、 PI3K、 p-GSK3β的作用(P < 0.05)。结论：Neu-P11、Mel能够提高胰岛素抵抗前脂肪细胞模型（3T3-L1细胞模型）中胰岛素受体后信号重要通路蛋白的表达，降低因信号通路蛋白异常导致的胰岛素抵抗，提高细胞膜蛋白对胰岛素的敏感性。Neu-P11、Mel通过和褪黑素受体2耦合来提高胰岛素受体后信号转导重要通路蛋白表达。 |
| 关键词: Neu-P11 褪黑素 胰岛素抵抗 p-IRS-1 PI3K p-GSK3β luzindole |
| DOI：10.16781/j.0258-879x.2016.09.1184 |
| 投稿时间：2015-09-04修订日期：2016-04-14 |
| 基金项目:湖南省教育厅科学研究项目（14C0909），湖南医药学院科学研究项目（2014KY02）. |
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| Effect of Neu-P11 on insulin signaling pathway in insulin-resistant adipocyte model |
| LI Xiu-ping1,CAI Shi-chang2*,YIN Wei-dong3,ZHANG Su-jun4,LU Qiong2,LI Xing2 |
| (College of Laboratory Medicine, Hunan University of Medicine, Huaihua 418000, Hunan, China;1. College of Laboratory Medicine, Hunan University of Medicine, Huaihua 418000, Hunan, China;Institute of Cardiovascular Disease, University of South China Medical College, Hengyang 412000, Hunan, China;Department of Experimental Animal, University of South China, Hengyang 412000, Hunan, China;Division of Basic Medical Sciences, Hunan University of Medicine, Huaihua 418000, Hunan, China) |
| Abstract: |
| Objective: The objective of present study was to examine the changes of melatonin receptor agonist Neu-P11 on expression of p-IRS-1/PI3K/p-GSK3β in 3T3-L1 adipocytes and to research the variation mechanisms, observe Neu-P11 improving insulin resistance because of p-IRS-1/PI3K/p-GSK3β abnormal expression of signaling pathways leading. Thereby, we can deeperly study the impact of Neu-p11 on theinsulin signaling pathway in adipocytes from insulin resistant mice.Methods: 3T3-L1 pre-adipocytes were cultivated and differentiated in adipogenic cocktailby IBMX, DEX and insulin; Confirm the establishment of insulin resistance model. The changes of p-IRS-1/PI3K/p-GSK3βprotein expressions before and after drug action were detected by Western blot; Results: Expression of Pp-IRS-1/PI3K/p-GSK3βreduced significantly by comparison with IS (P < 0.05). Melatonin and Neu-P11 can increase obviously the expression of p-IRS-1/PI3K/p-GSK3β(P < 0.05). But Luzindole can blockthe effect of melatonin, Neu-P11 increasing p-IRS-1/PI3K/p-GSK3β (P < 0.05).Conclusions: Melatonin and Neu-P11 can increase obviouslysignificant protein the expression of insulin receptor signaling pathway(P < 0.05). Neu-P11 and Mel improve important protein expression of insulin signaling pathway by coupling with melatonin receptor 2. |
| Key words: Neu-P11 melatonin insulin resistance p-IRS-1 PI3K p-GSK3β luzindole |
