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目的探讨2,2’,4,4’,5,5’-六氯联苯(PCB153)对体外培养胰岛β细胞株(INS-1)细胞毒性作用及机制。方法 PCB153设3个剂量组(1、3、6μmol/L),二甲基亚砜(DMSO)为溶剂对照组,染毒INS-1细胞24 h后,检测细胞存活率、凋亡、活性氧(ROS)水平、Caspase 3和Caspase 12等凋亡相关基因表达水平。结果 3、6μmol/LPCB153剂量组细胞存活率分别为(80.9±8.7)%和(42.2±4.3)%,与对照组比较均有下降(P<0.05);3μmol/LPCB153剂量组ROS为(9.2±0.4)、凋亡率为(30.7±3.4)%,6μmol/L PCB153剂量组ROS为(13.7±1.6)、凋亡率为(40.4±1.3)%,与对照组比较,ROS水平和细胞凋亡率均增加(P<0.05);与对照组比较,3μmol/L PCB153剂量组Caspase 3及3、6μmol/L PCB153剂量组Caspase 12基因表达水平均有增加(P<0.05)。结论 PCB153可诱导INS-1细胞凋亡,氧化应激和内质网信号通路可能参与PCB153对INS-1细胞的毒性作用。
Objective To investigate the cytotoxicity and mechanism of 2,2 ’, 4,4’, 5,5’-hexachlorobiphenyl (PCB153) on cultured islet β cell line (INS-1) in vitro. Methods PCB153 cells were treated with 3, 6 and 6 μmol / L dimethylsulfoxide (DMSO) for 24 h, and the cell viability, apoptosis, reactive oxygen species (ROS), Caspase 3, Caspase 12 and other apoptosis-related genes. Results The cell viability in 3,6 μmol / L PCB153 group was (80.9 ± 8.7)% and (42.2 ± 4.3)%, respectively, which was significantly lower than that in control group (P <0.05) 0.4). The apoptotic rate was (30.7 ± 3.4)%. The ROS level in PCB153 6μmol / L group was (13.7 ± 1.6) and the apoptosis rate was (40.4 ± 1.3)%. Compared with the control group, ROS level and apoptosis (P <0.05). Compared with the control group, the Caspase 3 and 3, 6μmol / L PCB153 dose 3μmol / L PCB153 dose group Caspase 12 gene expression levels were increased (P <0.05). Conclusion PCB153 can induce the apoptosis of INS-1 cells. Oxidative stress and endoplasmic reticulum signal pathways may be involved in the toxic effects of PCB153 on INS-1 cells.