Liu Liang, Wang Ran-Ping, Liu Xiao-Hong, Wang Lin-Xi, Liu Xiao-Ying, Chen Wen-Jia, Liu Li-Bin
Fujian Institute of Endocrinology, Department of Endocrinology, Union Hospital, Fujian Medical University, Fuzhou 350001, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2009 Nov;25(4):553-6.
To investigate the chronic effect of palmitic acid (PA) on apoptosis of pancreatic islet beta-cells and the possible mechanism.
Insulinoma cell line (MIN6 cells) were used in this study. After being incubated in PA (0.1 - 1.6 mml/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-FTTC/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.
Chronic PA dose-dependently (1) decreased the availability and increased the apoptosis of MIN6 cells; (2) decreased the phosphorylation of Akt and Bcl-2, but had no significant effects on Akt and Bax.
Chronic PA dose-dependently induced apoptosis of MIN6 cells, and this effect was possibly regulated by Akt/Bcl-2.
探讨棕榈酸(PA)对胰岛β细胞凋亡的慢性影响及其可能机制。
本研究采用胰岛素瘤细胞系(MIN6细胞)。将细胞在PA(0.1 - 1.6 mmol/L)中孵育24小时和48小时后,采用MTT法评估细胞活力。孵育48小时后,采用Hoechst-PI和Annexin-V-FTTC/PI流式细胞术评估各组细胞凋亡情况,采用蛋白质免疫印迹法检测p-Akt、Akt、Bax和Bcl-2的蛋白水平。
慢性PA呈剂量依赖性地(1)降低MIN6细胞活力并增加其凋亡;(2)降低Akt和Bcl-2的磷酸化水平,但对Akt和Bax无显著影响。
慢性PA呈剂量依赖性地诱导MIN6细胞凋亡,且该作用可能受Akt/Bcl-2调控。