| 线粒体及凋亡相关信号途径在脑缺血性损伤细胞死亡过程中的重要角色 |
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| 引用本文： | 代海滨,苗晓蕾,嵇 晴,段满林. 线粒体及凋亡相关信号途径在脑缺血性损伤细胞死亡过程中的重要角色[J]. 中国组织工程研究, 2015, 19(15): 2425-2430. DOI: 10.3969/j.issn.2095-4344.2015.15.025 |
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| 作者姓名： | 代海滨 苗晓蕾 嵇 晴 段满林 |
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| 作者单位： | 解放军第二军医大学南京临床医学院(南京军区南京总医院)麻醉科，江苏省南京市 210002 |
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| 基金项目： | 国家自然科学基金(81102514) |
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| 摘 要： | 背景：脑缺血后神经细胞病理变化的机制仍未完全阐明，现有的研究已经从细胞器水平，如线粒体等，深入研究其病理变化的机制。目的：总结和讨论线粒体及凋亡相关信号途径在脑缺血性损伤中的作用。方法：应用计算机检索CNKI和PubMed外文数据库，以“线粒体，凋亡，脑缺血，活性氧，再灌注，超氧化物歧化酶，一氧化氮合酶，Bcl-2蛋白家族，综述”为中文检索词，以“cerebral ischemia, mitochondrion, apoptosis，reactive oxygen species，reperfusion，superoxide dismutase，nitric oxide synthase，Bcl-2 protein family，review”为英文检索词，按纳入和排除标准对文献进行筛选，排除与研究目的无关和内容重复者，保留50篇文献做进一步分析。结果与结论：现有的研究表明，线粒体可通过产生大量活性氧，进而激活多种信号途径，及调控线粒体相关凋亡途径在脑缺血性损伤中起重要的作用。活性氧在脑缺血导致的细胞死亡中有重要作用，不仅引起生物大分子损伤，而且可引起凋亡信号转导。线粒体产生大量的活性氧，从而激活多种信号通路及参与凋亡的内在途径调控，在细胞死亡中起重要作用。中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程全文链接：
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| 关 键 词： | 组织构建 组织工程 线粒体 凋亡 脑缺血 活性氧 再灌注 超氧化物歧化酶 一氧化氮合酶 Bcl-2蛋白家族 国家自然科学基金 |
Neuronal mitochondria and apoptosis signaling pathways play an important role in cell death during transient cerebral ischemia |
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| Dai Hai-bin,Miao Xiao-lei,Ji Qing,Duan Man-lin. Neuronal mitochondria and apoptosis signaling pathways play an important role in cell death during transient cerebral ischemia[J]. Chinese Journal of Tissue Engineering Research, 2015, 19(15): 2425-2430. DOI: 10.3969/j.issn.2095-4344.2015.15.025 |
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| Authors: | Dai Hai-bin Miao Xiao-lei Ji Qing Duan Man-lin |
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| Affiliation: | Department of Anesthesiology, Nanjing Clinical Hospital of Second Military Medical University (Nanjing General Hospital of Nanjing Military Region), Nanjing 210002, Jiangsu Province, China |
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| Abstract: | BACKGROUND:Although the mechanism why neuronal cells will die after transient cerebral ischemia has not been completely elucidated, many researches nowadays have investigated the pathological mechanism in the level of cellular organs, such as mitochondria.OBJECTIVE:To summarize and discuss the functions of neuronal mitochondria and apoptosis signaling pathways in transient cerebral ischemia.METHODS:A computer-based online retrieval was performed to search papers in CNKI and PubMed databases using the key words of “cerebral ischemia, mitochondrion, apoptosis, reactive oxygen species, reperfusion, superoxide dismutase, nitric oxide synthase, Bcl-2 protein family, review” in Chinese and English, respectively. Papers published recently or in the prestigious journals were selected in the same field. After excluding objective-independent papers and repeated studies, 50 papers were included for further analysis.RESULTS AND CONCLUSION:Recently mitochondria are found to play an important role after transient cerebral ischemia by producing a lot of reactive oxygen species to activate many kinds of signaling pathways and regulate mitochondria-mediated apoptosis. Reactive oxygen cannot only induce biomacromolecule injury but also induce apoptosis signal transduction. Deeply investigation is needed on the pathological mechanism after transient cerebral ischemia. |
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| Keywords: | Tissue Engineering Mitochondria Apoptosis Brain Ischemia |
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