微囊藻毒素-LR通过线粒体途径诱导人支气管上皮细胞凋亡  被引量:1

Apoptosis Induced by Microcystin-LR in Human Bronchial Epithelial Cell through Mitochondrial Pathway

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作  者:薛利剑[1] 刘晓蕙[2] 杨明峰[1] 刘迎[1] 朱靖[1] 乔豆 庄东刚[1] 崔留欣[1] 张慧珍[1] 

机构地区:[1]郑州大学公共卫生学院,郑州450001 [2]河南中医学院基础医学院,郑州450046

出  处:《生态毒理学报》2015年第3期123-128,共6页Asian Journal of Ecotoxicology

基  金:国家自然科学基金(81472948);河南省科技攻关计划(142102310344);河南省科技发展计划(132102310051);河南省科技重点攻关项目(122102310208);河南省高等学校青年骨干教师资助计划(2011GGJS-012)

摘  要:探讨线粒体Caspase依赖性途径是否参与微囊藻毒素-LR(microcystin-LR,MC-LR)诱导人支气管上皮细胞(human bronchial epithelial cells,16HBE)凋亡过程。将处于对数生长期的16HBE分别暴露于终浓度为0(对照组)、2.5、5、10μg·m L-1的微囊藻毒素-LR和10μg·m L-1MC-LR+50μmol·L-1Caspase广谱抑制剂Z-VAD-FMK,持续24 h和48 h。检测细胞凋亡率,线粒体跨膜电位(ΔΨm),Caspase-3和Caspase-9相对表达量。结果显示,与对照组相比,各浓度染毒组细胞凋亡率和Caspase-3、Caspase-9相对表达量均升高,10μg·m L-1MC-LR染毒组线粒体膜电位降低;与10μg·m L-1MC-LR组相比,10μg·m L-1MCLR+50μmol·L-1Z-VAD-FMK组细胞凋亡率明显降低,Caspase-3和Caspase-9相对表达量降低,差异均有统计学意义(P<0.05)。且随着MC-LR染毒浓度的升高或染毒时间的延长,16HBE细胞凋亡率和Caspase-3、Caspase-9相对表达量呈升高趋势。研究表明,MC-LR可以通过线粒体Caspase依赖性途径诱导16HBE细胞凋亡。To verify that mitochondrial Caspase-dependent pathway is involved in apoptosis in human bronchial epithelial cells induced by microcystin-LR (MC-LR), the logarithmic phase 16HBE cells were exposed to final con- centrations of 0(control group), 2.5, 5, 10 t^g'mLI MC-LIL as well as 10 μg·mL-1MC-LR and 50 μmol·L-1 Z-VAD- FMK (a broad-spectrum Caspase inhibitor) for 24 h or 48 h in vitro. The apoptosis rate, rnitochondrial membrane potential (AWm), and the expression of Caspase-3 and Caspase-9 were detected. Compared with the control group,the apoptosis rate, the expression levels of Caspase-3 and Caspase-9 increased significantly (P〈l0.05) in the treat- ment groups, and the △ψm decreased markedly (P〈0.05) in the group treated with 10 ptg-mL @ MC-LR. The apop- tosis rate, the expression levels of Caspase-3 and Caspase-9 in the group treated with both 10 tzg.mL -1 MC-LR and 50/zmol-L 1Z-VAD-FMK were lower than that in the group treated only with the 10μg. mL-1 MC-LR. In addition, the apoptosis rates, the expression levels of Caspase-3 and Caspase-9 had a positive correlation with MC-LR con- centrations and treatment time. These results suggested that MC-LR can induce 16HBE cells apoptosis through the mitochondrial Caspase-dependent pathway.

关 键 词:微囊藻毒素-LR 线粒体途径 人支气管上皮细胞 凋亡 

分 类 号:X171.5[环境科学与工程—环境科学]

 

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