| 崔 佳,段佳林,王 磊,曹珊珊,贾 娜,文爱东.竹节参皂苷IVa通过Akt/mTOR通路保护胰岛β细胞损伤[J].,2018,(17):3224-3229 |
| 竹节参皂苷IVa通过Akt/mTOR通路保护胰岛β细胞损伤 |
| Protective Effects of Chikusetsu Saponin Ⅳa on Pancreatic β Cells Injuryed by High Glucose |
| 投稿时间：2018-04-09 修订日期：2018-05-04 |
| DOI：10.13241/j.cnki.pmb.2018.17.005 |
| 中文关键词: 竹节参皂苷IVa 葡萄糖毒性 Akt/mTOR 胰岛素释放 |
| 英文关键词: Chikusetsu saponin Ⅳa Glucose toxicity Akt/mTOR Insulin release |
| 基金项目:国家自然科学基金项目（81603350）；陕西省中医药管理局项目（JCMS056）；西京医院助推计划项目（XJZT15M19） |
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| 中文摘要: |
| 摘要 目的：研究竹节参皂苷IVa（CHS）对高糖诱导的胰岛β细胞损伤的保护作用及其作用机制。方法：采用高糖建立胰岛β细胞损伤模型，分为正常组、模型组、CHS给药低、中和高剂量组（25、50 和100 μM）。MTT法检测CHS对胰岛细胞存活率的影响，胰岛素释放实验检测CHS对胰岛β细胞功能的影响，试剂盒检测Caspase 3和细胞色素c的水平，蛋白印迹法检测Bax、Bcl-2、Akt、mTORC1、S6K蛋白表达和磷酸化水平变化。结果：与正常组比较，高糖使INS-1细胞存活率降低，胰岛素释放减少，同时Caspase-3，细胞色素c，Bax蛋白表达增加，Bcl-2蛋白表达减少；与模型组比较，CHS可以明显逆转这一趋势（P <0.05）。此外，CHS可剂量依赖性的促进Akt，mTORC1和S6K磷酸化水平，进一步研究发现，CHS保护胰岛INS-1细胞的作用及对mTORC1和S6K磷酸化的作用被siAkt抵消。结论：CHS可以对抗胰岛β细胞的糖毒性，降低胰岛INS-1细胞凋亡，增加胰岛素释放水平，其作用机制可能与激活Akt/mTOR信号通路有关。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the protective effects of Chikusetsu saponin Ⅳa on islet β cells injured by high glucose. Methods: High glucose was used to induce injury in islet β cells, and divided into Control, Model, low, middle and high treatment groups (25, 50 and 100 μM). MTT was used to measure the effect of CHS on cells survival rate. Insulin release assay experiment was used to de- tect the insulin release effect of CHS on islet β cell function. Caspase 3 and cytochrome c levels were measured by the kit, the expression of Bax and Bcl-2 were measured by western blotting, and also the phosphorylation levels of Akt, mTROC1 and S6K. Results: Compared with the model group, CHS significantly increased the survival rate, induced the releasing level of insulin, decreased the ex- pression of Caspase-3, cytochrome c and Bax, increased the expression of Bcl-2, and also raised the ratio of Bcl-2/Bax (P<0.05). Addi- tionally, CHS could increase the phosphorylation levels of Akt, mTROC1 and S6K in a dose dependent manner. In further studies, we found that the protective effects of CHS and the effect of inducing mTROC1 and S6K phosphorylation were all abolished by siAkt. Conclusion: CHS protected cells from cell injury caused by high glucose, decreased cell apoptosis, increased insulin release levels. The possible mechanism might through activating Akt/mTOR signaling pathway. |
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