| 张 娟,赵 原,赵晓宏,周庆元,李晓苗.PTEN参与小檗碱保护脂毒性损伤的胰岛βTC3细胞[J].现代生物医学进展英文版,2017,17(5):810-814. |
| PTEN参与小檗碱保护脂毒性损伤的胰岛βTC3细胞 |
| PTEN Gene Participated in Protective Effects of Berberine on Lipoapoptosis in Pancreatic βTC3 Cells |
| Received:March 31, 2016 Revised:April 14, 2016 |
| DOI：10.13241/j.cnki.pmb.2017.05.003 |
| 中文关键词: 小檗碱 棕榈酸 胰岛βTC3细胞 胰岛素分泌 PTEN |
| 英文关键词: Berberine Palmic acid Pancreatic βTC3 cells Insulin secretion PTEN |
| 基金项目:国家自然科学基金项目(81573746)；陕西省卫计委2014课题（2014D67） |
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| 中文摘要: |
| 摘要 目的：探讨小檗碱保护棕榈酸诱导的胰岛βTC3细胞的可能机制，观察PTEN是否参与该过程，以及小檗碱对胰岛素分泌的影响。方法：用1.0 mmol/L棕榈酸制作胰岛βTC3细胞脂毒性损伤模型，给予小檗碱干预；放射免疫法检测胰岛素分泌，West- ern blot法进行PTEN、p-AKT、AKT、Bcl-2、Bax、活性Caspase3蛋白的检测。实验分3大组（对照组、棕榈酸组、棕榈酸+小檗碱治疗组），棕榈酸分别作用3个时间段（24、48、72 h）。结果：①放射免疫法胰岛素分泌测定结果显示：β细胞暴露于棕榈酸24 h后，5.6、16.7 mmol/L葡萄糖刺激的胰岛素分泌均较正常对照组显著减少（P＜0.01）；添加小檗碱干预后胰岛素分泌较棕榈酸组回升，但较对照组减少（P均＜0.01）。②在棕榈酸处理的3个时间段内，与对照组相比，棕榈酸组的PTEN、Bax、Active-Caspase3蛋白表达水平显著升高，p-AKT、Bcl-2蛋白水平下降；小檗碱干预后PTEN、Bax蛋白表达水平下降，p-AKT、Bcl-2蛋白水平提高（P均＜0.01）。结论：小檗碱可改善棕榈酸引起的胰岛素分泌减少，抑制脂毒性诱导的PTEN表达增加，减少促凋亡基因Bax、Active-Cas- pase3表达，并增加抑凋亡基因Bcl-2基因表达及AKT的活化，从而拮抗棕榈酸诱导的β细胞凋亡，保护?茁细胞功能。 |
| 英文摘要: |
| ABSTRACT Objective: To evaluate the protective effect of berberine on pancreatic βTC3 cells lipoapoptosis induced by free fatty acids, investigated the role of PTEN/AKT signaling in berberine involved beta cell protection. To explore the anti-diabetic effects of berberine and its influence on inslin secretion. Methods: The basal and glucose stimulated insulin secretion capability of βTC3 cells were evaluated when exposed to FFAs with or without berberine by Radioimmunoassay. The expression of PTEN, AKT, p-AKT and apoptosis related proteins Bax, Bcl-2 and Active-Caspase3 were detected by western blotting in βTC3 cells when exposed to FFAs with or without berberine. Results: Berberine substantially facilitated the basal and glucose stimulated insulin secretion of beta cells in high FFAs condi- tion. Western blot revealed that the phosphorylation of AKT and Bcl-2 was markedly decreased under lipid stress but was elevated when treated with berberine. Moreover, FFAs could up-regulate the expression levels of PTEN, Bax, and Active-Caspase3, but down-regulate the expression levels of p-AKT and Bcl-2 in beta cells, which were canceled by the addition of berberine. Conclusion: Berberine observ- ably inhibited the apoptosis, elevated proliferation and the basal and glucose stimulated insulin secretion of beta cells in high FFAs condi- tion. Furthermore, the protective action of berberine was probability mediated by activation of PTEN/AKT, which was accompanied by the down-regulation of Bax, Active-Caspase3 and up-regulation of p-AKT and Bcl-2 expressions. |
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