| 硫化氢对化学性缺氧诱导PC12细胞凋亡的影响 |
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| 引用本文： | 孟金兰,兰爱平,郭瑞鲜,杨春涛,杨战利,黄雪,冯鉴强. 硫化氢对化学性缺氧诱导PC12细胞凋亡的影响[J]. 中山大学学报(医学科学版), 2010, 31(1): 79-84 |
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| 作者姓名： | 孟金兰 兰爱平 郭瑞鲜 杨春涛 杨战利 黄雪 冯鉴强 |
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| 作者单位： | 1. 广东药学院生理教研室, 广东 广州 510006; 2. 中山大学中山医学院生理教研室, 广东 广州 510080; 3. 中山大学附属第一医院心血管内科, 广东 广州 510080 |
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| 摘 要： | 【目的】 探讨硫化氢(H2S)对抗二氯化钴(CoCl2)诱导PC12细胞凋亡的作用及其初步机制｡【方法】 应用化学性缺氧模拟剂CoCl2在PC12细胞建立化学性缺氧损伤模型;以硫氢化钠(NaHS)作为H2S的供体;应用CCK-8比色法检测细胞存活率;碘化丙啶(PI)染色流式细胞技术(FCM)检测细胞凋亡率; Hoechst33258 染色检测细胞凋亡的形态学变化; 罗丹明123(Rh123) 染色荧光显微镜照相检测细胞线粒体膜电位(MMP); 2’,7’-二氯荧光黄双乙酸盐(DCFH-DA)染色荧光显微镜照相检测细胞内的活性氧 (ROS)水平｡【结果】 CoCl2引起PC12细胞的存活率显著降低及凋亡率明显增加, 同时引起PC12细胞的MMP 明显降低及ROS 生成显著增加｡在600 μmol/L CoCl2处理PC12细胞前,应用100 ~ 400 μmol/L NaHS 预处理30 min,呈浓度依赖性地阻断CoCl2引起PC12细胞的存活率降低; 200 μmol/L､400 μmol/L NaHS 预处理能显著地降低600 μmol/L CoCl2 引起PC12 细胞的凋亡率增加并阻断CoCl2 引起的MMP降低及ROS升高｡【结论】 H2S 具有神经细胞保护作用, 能明显地对抗CoCl2诱导的PC12细胞凋亡,此作用可能与其减少ROS生成,提高MMP有关｡
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| 关 键 词： | 硫化氢 二氯化钴 缺氧 PC12细胞 凋亡 |
| 收稿时间： | 2009-07-22; |
Effects of Hydrogen Sulfide on Apoptosis of PC12 Cells Induced by Chemical Hypoxia |
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| MENG Jin-lan,LAN Ai-ping,GUO Rui-xian,YANG Chun-tao,YANG Zhan-li,HUANG xue,FENG Jian-qiang. Effects of Hydrogen Sulfide on Apoptosis of PC12 Cells Induced by Chemical Hypoxia[J]. Journal of Sun Yatsen University(Medical Sciences), 2010, 31(1): 79-84 |
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| Authors: | MENG Jin-lan LAN Ai-ping GUO Rui-xian YANG Chun-tao YANG Zhan-li HUANG xue FENG Jian-qiang |
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| Affiliation: | MENG Jin-lan1,2,LAN Ai-ping2,GUO Rui-xian2,YANG Chun-tao2,YANG Zhan-li2,HUANG xue3,FENG Jian-qiang2 (1.Department of Physiology,Guangdong Pharmaceutical University,Guangzhou 510006,China,2.Department of Physiology,Zhongshan Medical College,Sun Yat-sen University,Guangzhou 510080,3.Department of Cardiovasology,The First Afilliated Hospital,China) |
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| Abstract: | [Objective] To explore the cytoprotecfion of hydrogen sulfide (H_2S) against cobalt chloride (CoCl_2)-induced apeptosis in PC12 cells and the underlying mechanisms. [Methods] CoCl_2 (a chemical hypoxia-mimetic agent) was used to establish the chemical hypoxia-induced PC12 cell injuries model. Sodium hydrosulfide (NaHS) was used as a H_2S donor. The viability of PC12 cells was measured by CCK-8 assay. The percentage of apeptotic cells was assessed by propidium iodide stain flow cytometry (FCM). The morphological change of apeptotic cells was tested by using the chromatin dye Hoechst 33258. The mitochondrial membrane potential (MMP) was analyzed by rhodamine 123 staining and photofluorography. The level of reactive oxygen species (ROS) in PC12 cells was measured by DCFH-DA staining and photofluorography. [Results] CoCl_2 induced a decrease in cell viability and an increase in percentage of apeptosis in PC12 cells along with dissipation of MMP as well as overproduction of ROS. When PC12 cells were treated with Naris 30 min before CoCl_2 treatment a decrease in viability of PC12 cells induced by 600 μmol/L CoCl_2 was concentration-dependently blocked by NaHs (100, 200, and 400 μmol/L). Pretreatment with NaHS at 200 and 400 μmol/L obviously reduced the apepetotic percentage of PC12 cells induced by 600 μmol/L CoCl_2 and inhibited the dissipation of MMP and overproduction of ROS. [Conclusion] H_2S protected PC12 cells against CoCl_2-induced apeptosis, which may be associated with the inhibition of H_2S on the dissipation of MMP and overproduction of ROS induced by CoCl_2. |
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| Keywords: | hydrogen sulfide cobalt chloride hypoxia PC12 cells apeptosis |
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