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作 者:刘亮[1] 王燕萍[1] 刘晓红[1] 王林曦[1] 刘小莺[1] 陈闻佳[1] 刘礼斌[1]
机构地区:[1]福建医科大学附属协和医院内分泌科,福建省内分泌研究所,福建福州350001
出 处:《中国应用生理学杂志》2009年第4期553-556,共4页Chinese Journal of Applied Physiology
基 金:福建省高校新世纪优秀人才项目(NCETFJ0703)
摘 要:目的:探讨软脂酸(PA)对胰岛β细胞(MIN6细胞)凋亡及Akt信号途径的影响。方法:细胞采用小鼠胰岛素瘤细胞株MIN6,不同浓度PA(0-1.6mmol/L)干预24、48 h,MTT法测定各组细胞存活率。干预48 h后Hoechst-PI染色法和Annexin-Ⅴ/PI双标流式测定法测定各组细胞凋亡率,Western-blot法测定p-Akt、Akt、Bax、Bcl-2。结果:随着PA浓度的增高①MIN6细胞存活率逐渐减小、凋亡率逐渐增大;②MIN6细胞中p-Akt和Bcl-2的表达逐渐减少,而Akt、Bax无明显改变。结论:长时间PA作用引起MIN6细胞凋亡,并呈现一定的量效关系;这一效应可能是通过Akt/Bcl-2产生作用的。Aim: To investigate the chronic effect of palmitic acid (PA) on apoptosis of pancreatic islet β-cells and the possible mechanism. Methods: Insulinoma cell line(MIN6 cells) were used in this study. After being incubated in PA(0.1 - 1.6mml/L) for 24 and 48 hours, MTT method was used to evaluate the livability. After being incubated for 48 h, Hoechst-PI and Annexin-V-FITC/PI FACS were used to estimate the apoptosis in each group, Western-blotting assay was used to estimate the protein level of p-Akt, Akt, Bax and Bcl-2. Results: Chronic PA dose-dependently ①decreased the availability and increased the apoptosis of MIN6 cells; ②decreased the phosphorylation of Akt and Bcl-2, but had no significant effects on Akt and Bax. Conclusion: Chronic PA dose-dependently induced apoptosis of MIN6 cells, and this effect was possibly regulated by Akt/Bcl-2.
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