留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码
x 关闭 永久关闭

应中央军委要求，2022年9月起，《药学实践杂志》将更名为《药学实践与服务》，双月刊，正文96页；2023年1月起，拟出版月刊，正文64页，数据库收录情况与原《药学实践杂志》相同。欢迎作者踊跃投稿！

脑缺血和再灌注损伤与防治机制的研究进展

吴金华,  马慧萍,  蒙萍,  贾正平

downloadPDF
文章导航 > 药学实践与服务  > 2014 >  32(6): 401-404,447
吴金华, 马慧萍, 蒙萍, 贾正平. 脑缺血和再灌注损伤与防治机制的研究进展[J]. 药学实践与服务, 2014, 32(6): 401-404,447. doi: 10.3969/j.issn.1006-0111.2014.06.001
引用本文: 吴金华, 马慧萍, 蒙萍, 贾正平. 脑缺血和再灌注损伤与防治机制的研究进展[J]. 药学实践与服务, 2014, 32(6): 401-404,447. doi: 10.3969/j.issn.1006-0111.2014.06.001
shu
WU Jinhua, MA Huiping, MENG Ping, JIA Zhengping. Mechanisms of damage and treatments of cerebral ischemia and reperfusion[J]. Journal of Pharmaceutical Practice and Service, 2014, 32(6): 401-404,447. doi: 10.3969/j.issn.1006-0111.2014.06.001
Citation: WU Jinhua, MA Huiping, MENG Ping, JIA Zhengping. Mechanisms of damage and treatments of cerebral ischemia and reperfusion[J]. Journal of Pharmaceutical Practice and Service, 2014, 32(6): 401-404,447. doi: 10.3969/j.issn.1006-0111.2014.06.001
shu

脑缺血和再灌注损伤与防治机制的研究进展

doi: 10.3969/j.issn.1006-0111.2014.06.001
  • 1.

    兰州军区兰州总医院, 甘肃 兰州 730050;兰州大学药学院, 甘肃 兰州 730000

  • 2.

    兰州军区兰州总医院, 甘肃 兰州 730050

基金项目: 国家科技部重大专项资助项目(2008ZXJ09014-010);甘肃省省自然科学研究基金计划项目(1107RJZA100);全军医药卫生科研基金课题(CLZ11JA06).

Mechanisms of damage and treatments of cerebral ischemia and reperfusion

  • 1.

    Lanzhou General Hospital, Lanzhou Region of PLA, Lanzhou 730050, China;School of Pharmacy, Lanzhou University, Lanzhou 730000, China

  • 2.

    Lanzhou General Hospital, Lanzhou Region of PLA, Lanzhou 730050, China

  • 摘要: 总结脑缺血和再灌注损伤的发生和防治机制的研究进展,展望未来研究趋势。采用文献归纳总结的方法进行分析。脑缺血和再灌注造成的损伤与炎性反应、细胞内Ca2+超载、自由基的迅速增加、兴奋性氨基酸的大量释放等因素有关。防治脑缺血和再灌注损伤的机制主要有缩短缺血时间、阻断谷氨酸受体偶联的Na+和Ca2+内流、清除自由基、抑制凋亡、减轻炎症反应、促进神经元生长与修复等多个方面。多靶点联合治疗可能是防治脑缺血和再灌注损伤的一个方向。
    Abstract: To summarize the advances in mechanisms of damage and treatments of cerebral ischemia and reperfusion and forecasts future research directions.The existing achievements in literatures were summarized.Cerebral ischemia and reperfusion damage were related to inflammatory response, intracellular calcium overload, free radicals injury, release of excitatory amino acids and other factors. The treatments included reducing ischemia time, blocking glutamate receptors, free radical scavenging, inhibition of apoptosis, reducing inflammation, and promoting neuronal growth, etc. Multi-target treatment would be future directions in treatment of cerebral ischemia.
  • [1] Doyle KP, Simon RP, Stenzel-Poore MP. Mechanisms of ischemic brain damage[J].Neuropharmacology, 2008, 55(3): 310-318.
    [2] Yager JY, Ashwal S. Animal models of perinatal hypoxic-ischemic brain damage[J].Pedietr Neurol,2009, 40(3): 156-167.
    [3] Huang L, Chen N, Ge M, et al. Ca2+ and acidosis synergistically lead to the dysfunction of cortical GABAergic neurons during ischemia[J].Bioch Biophys Res Commun, 2010, 394(3): 709-714.
    [4] Zhang YF, Fan XJ, Li X, et al. Ginsenoside Rg1 protects neurons from hypoxic-ischemic injury possibly by inhibiting Ca2+ influx through NMDA receptors and L-type voltage-dependent Ca2+ channels[J].Eur J Pharmacol, 2008, 586(1-3): 90-99.
    [5] Szydlowska K, Tymianski M. Calcium, ischemia and excitotoxicity[J].Cell Calcium, 2010, 47(2): 122-129.
    [6] Gouriou Y, Demaurex N, Bijlenga P, et al. Mitochondrial calcium handling during ischemia-induced cell death in neurons[J].Biochimie, 2011, 93(12): 2060-2067.
    [7] Richard MJ, Connell BJ, Khan BV, et al. Cellular mechanisms by which lipoic acid confers protection during the early stages of cerebral ischemia: a possible role for calcium[J].Neurosci Res, 2011, 69(4): 299-307.
    [8] Xu J, Liu ZA, Pei DS, et al. Calcium/calmodulin-dependent kinase II facilitated GluR6 subunit serine phosphorylation through GluR6-PSD95-CaMKII signaling module assembly in cerebral ischemia injury[J].Brain Res, 2010, 1366: 197-203.
    [9] Hurtado O, Moro MA, Cardenas A, et al. Neuroprotection afforded by prior citicoline administration in experimental brain ischemia: effects on glutamate transport[J].Neurobiol Dis 2005, 18(2): 336-345.
    [10] Arranz AM, Gottlieb M, Perez-Cerda F, et al. Increased expression of glutamate transporters in subcortical white matter after transient focal cerebral ischemia[J].Neurobiol Dis, 2010, 37(1): 156-165.
    [11] Wang L, Deng S, Lu Y, et al. Increased inflammation and brain injury after transient focal cerebral ischemia in activating transcription factor 3 knockout mice[J].Neuroscience, 2012, 220: 100-108.
    [12] Ye XH, Wu Y, Guo PP, et al. Lipoxin A4 analogue protects brain and reduces inflammation in a rat model of focal cerebral ischemia reperfusion[J].Brain Res, 2010, 1323: 174-183.
    [13] Webster CM, Kelly S, Koike MA, et al. Inflammation and NFkappaB activation is decreased by hypothermia following global cerebral ischemia[J].Neurobiol Dis, 2009, 33(2): 301-312.
    [14] del Zoppo GJ. Inflammation and the neurovascular unit in the setting of focal cerebral ischemia[J].Neuroscience, 2009, 158(3): 972-982.
    [15] Kim BJ, Kim MJ, Park JM, et al. Reduced neurogenesis after suppressed inflammation by minocycline in transient cerebral ischemia in rat[J].J Neurol Sci, 2009, 279(1-2): 70-75.
    [16] Corsani L, Bizzoco E, Pedata F, et al. Inducible nitric oxide synthase appears and is co-expressed with the neuronal isoform in interneurons of the rat hippocampus after transient ischemia induced by middle cerebral artery occlusion[J].Exp Neurol, 2008, 211(2): 433-440.
    [17] Mohammadi MT, Shid-Moosavi SM, Dehghani GA. Contribution of nitric oxide synthase (NOS) in blood-brain barrier disruption during acute focal cerebral ischemia in normal rat[J].Pathophysiology, 2012, 19(1): 13-20.
    [18] Kubo K, Nakao S, Jomura S, et al. Edaravone, a free radical scavenger, mitigates both gray and white matter damages after global cerebral ischemia in rats[J].Brain Res, 2009, 1279: 139-146.
    [19] Nurmi A, Miettinen TK, Puolivali J, et al. Neuroprotective properties of the non-peptidyl radical scavenger IAC in rats following transient focal cerebral ischemia[J].Brain Res, 2008, 1207: 174-181.
    [20] Cunningham LA, Wetzel M, Rosenberg GA. Multiple roles for MMPs and TIMPs in cerebral ischemia[J].Glia, 2005, 50(4): 329-339.
    [21] Rosenberg GA. Matrix metalloproteinases in neuroinflammation[J].Glia,2002, 39(3): 279-291.
    [22] Xu L, Xiong X, Ouyang Y, et al. Heat shock protein 72 (Hsp72) improves long term recovery after focal cerebral ischemia in mice[J].Neurosci Lett, 2011, 488(3): 279-282.
    [23] Qi D, Liu H, Niu J, et al. Heat shock protein 72 inhibits c-Jun N-terminal kinase 3 signaling pathway via Akt1 during cerebral ischemia[J].J Neurol Sci, 2012, 317(1-2): 123-129.
    [24] Stetler RA, Gan Y, Zhang W, et al. Heat shock proteins: cellular and molecular mechanisms in the central nervous system[J].Prog Neurobiol, 2010, 92(2): 184-211.
    [25] Barreto GE, White RE, Xu L, et al. Effects of heat shock protein 72 (Hsp72) on evolution of astrocyte activation following stroke in the mouse[J].Exp Neurol, 2012, 238(2): 284-296.
    [26] Muhammad S, Barakat W, Stoyanov S, et al. The HMGB1 receptor RAGE mediates ischemic brain damage[J].J Neurosci, 2008, 28(46): 12023-12031.
    [27] Chang WJ, Toledo-Pereyra LH. The role of HMGB1 and HSP72 in ischemia and reperfusion injury[J].J Surg Res, 2011, 166(2): 219-221.
    [28] Strbian D, Durukan A, Pitkonen M, et al. The blood-brain barrier is continuously open for several weeks following transient focal cerebral ischemia[J].Neuroscience, 2008, 153(1): 175-181.
    [29] Mohagheghi F, Bigdeli MR, Rasoulian B, et al. The neuroprotective effect of olive leaf extract is related to improved blood-brain barrier permeability and brain edema in rat with experimental focal cerebral ischemia[J].Phytomedicine, 2011, 18(2-3): 170-175.
    [30] Xiong ZG, Zhu XM, Chu XP, et al. Neuroprotection in ischemia: blocking calcium-permeable acid-sensing ion channels[J].Cell, 2004, 118(6): 687-698.
    [31] Pandey AK, Hazari PP, Patnaik R, et al. The role of ASIC1a in neuroprotection elicited by quercetin in focal cerebral ischemia[J].Brain Res, 2011, 1383: 289-299.
    [32] Lee BK, Lee DH, Park S, et al. Effects of KR-33028, a novel Na+/H+ exchanger-1 inhibitor, on glutamate-induced neuronal cell death and ischemia-induced cerebral infarct[J].Brain Res, 2009, 1248: 22-30.
    [33] Kim YR, Kim HN, Jang JY, et al. Electroacupuncture confers beneficial effects through ionotropic glutamate receptors involving phosphatidylinositol-3 kinase/Akt signaling pathway in focal cerebral ischemia in rats[J].Eur J Integrat Med, 2012, 4(4): e413-e420.
    [34] Im DS, Jeon JW, Lee JS, et al. Role of the NMDA receptor and iron on free radical production and brain damage following transient middle cerebral artery occlusion[J].Brain Res, 2012, 1455: 114-123.
    [35] Benakis C, Bonny C, Hirt L. JNK inhibition and inflammation after cerebral ischemia[J].Brain Behav Immun, 2010, 24(5): 800-811.
    [36] Emanueli C. Nerve growth factor promotes angiogenesis and ateriogenesis in ischemic hindlimbs[J]. Circulation, 2002, 106(17): 2257-2262.
  • [1] 陈静, 何瑞华, 翁月, 徐熠, 刘静, 黄瑾.  基于网络药理学和分子对接技术探究定清片活性成分治疗白血病的作用机制 . 药学实践与服务, 2024, 42(11): 479-486. doi: 10.12206/j.issn.2097-2024.202401073
    [2] 陈金涛, 乔子婴, 马明华, 张若曦, 王振伟, 年华.  基于网络药理学和分子对接技术研究金芪清疏颗粒治疗社区获得性肺炎的潜在机制 . 药学实践与服务, 2024, 42(11): 471-478. doi: 10.12206/j.issn.2097-2024.202312014
    [3] 张广雨, 杜晶, 刘梦珍, 朱丹妮, 闫慧, 刘冲.  新斯的明与山莨菪碱联合应用对肺型氧中毒的保护作用及其机制的研究 . 药学实践与服务, 2024, 42(10): 433-438, 444. doi: 10.12206/j.issn.2097-2024.202310049
    [4] 岳春华, 贲永光, 王海桥.  基于NLRP1炎症小体探讨百合知母汤抗抑郁的作用机制 . 药学实践与服务, 2024, 42(8): 325-333. doi: 10.12206/j.issn.2097-2024.202401033
    [5] 修建平, 杨朝爱, 刘禧澳, 潘乾禹, 韦广旭, 王卫星.  全反式维甲酸对肝星状细胞活化及氧化应激的作用和机制探索 . 药学实践与服务, 2024, 42(7): 291-296. doi: 10.12206/j.issn.2097-2024.202312054
    [6] 景凯, 杨慈荣, 张圳, 臧艺蓓, 刘霞.  黄芪甲苷衍生物治疗慢性心力衰竭小鼠的药效评价及作用机制研究 . 药学实践与服务, 2024, 42(5): 190-197. doi: 10.12206/j.issn.2097-2024.202310004
    [7] 钱淑雨, 李铁军.  耐碳青霉烯类肠杆菌耐药机制的研究进展 . 药学实践与服务, 2024, 42(10): 419-425. doi: 10.12206/j.issn.2097-2024.202405005
    [8] 杨彬, 王作君, 陈菡, 张敬一.  基于DRGs的医院合理用药管理机制探索实践 . 药学实践与服务, 2024, 42(): 1-5. doi: 10.12206/j.issn.2097-2024.202404030
    [9] 李清, 郭宜银, 陈颖, 瞿发林, 董文燊, 戈煜.  夜宁胶囊对小鼠镇静催眠作用及其机制的研究 . 药学实践与服务, 2024, 42(8): 346-349. doi: 10.12206/j.issn.2097-2024.202211047
    [10] 徐飞, 陈瑾, 鲁育含, 李志勇.  肠道菌群参与糖尿病肾病的机制研究进展 . 药学实践与服务, 2024, 42(5): 181-184, 197. doi: 10.12206/j.issn.2097-2024.202312023
    [11] 陈莹, 许子华, 胡北, 崔亚玲, 高欢, 吴琼.  通便灵胶囊治疗便秘的药效与机制研究 . 药学实践与服务, 2024, 42(): 1-7. doi: 10.12206/j.issn.2097-2024.202404008
    [12] 迟文雅, 袁艳, 李伟林, 吴茼妤, 俞媛.  负载骨髓间充质干细胞/白藜芦醇脂质体的水凝胶支架用于创伤性脑损伤治疗 . 药学实践与服务, 2024, 42(): 1-8. doi: 10.12206/j.issn.2097-2024.202406034
    [13] 李想, 陆鸿远, 张明玉, 高欢, 姚东, 许子华.  米格列醇激活UCP1介导棕色脂肪对冷暴露小鼠损伤的研究 . 药学实践与服务, 2024, 42(): 1-6. doi: 10.12206/j.issn.2097-2024.202404005
    [14] 张岩, 李炎君, 刘家荟, 邓娇, 原苑, 张敬一.  药物性肝损伤不良反应分析 . 药学实践与服务, 2024, 42(): 1-5. doi: 10.12206/j.issn.2097-2024.202404034
    [15] 姜涛, 徐卫凡, 蒋益萍, 夏天爽, 辛海量.  巴戟天丸组方对Aβ损伤成骨细胞的作用及基于网络药理学的机制研究 . 药学实践与服务, 2024, 42(7): 285-290, 296. doi: 10.12206/j.issn.2097-2024.202305011
  • 加载中
WeChat 点击查看大图
计量
  • 文章访问数:  4259
  • HTML全文浏览量:  715
  • PDF下载量:  161
  • 被引次数: 0
出版历程
  • 收稿日期:  2013-06-07
  • 修回日期:  2013-12-20

脑缺血和再灌注损伤与防治机制的研究进展

doi: 10.3969/j.issn.1006-0111.2014.06.001
  • 1. 兰州军区兰州总医院, 甘肃 兰州 730050;兰州大学药学院, 甘肃 兰州 730000
  • 2. 兰州军区兰州总医院, 甘肃 兰州 730050
    • 基金项目:  国家科技部重大专项资助项目(2008ZXJ09014-010);甘肃省省自然科学研究基金计划项目(1107RJZA100);全军医药卫生科研基金课题(CLZ11JA06).
  • 收稿日期: 2013-06-07
  • 修回日期: 2013-12-20

摘要: 总结脑缺血和再灌注损伤的发生和防治机制的研究进展,展望未来研究趋势。采用文献归纳总结的方法进行分析。脑缺血和再灌注造成的损伤与炎性反应、细胞内Ca2+超载、自由基的迅速增加、兴奋性氨基酸的大量释放等因素有关。防治脑缺血和再灌注损伤的机制主要有缩短缺血时间、阻断谷氨酸受体偶联的Na+和Ca2+内流、清除自由基、抑制凋亡、减轻炎症反应、促进神经元生长与修复等多个方面。多靶点联合治疗可能是防治脑缺血和再灌注损伤的一个方向。

English Abstract

吴金华, 马慧萍, 蒙萍, 贾正平. 脑缺血和再灌注损伤与防治机制的研究进展[J]. 药学实践与服务, 2014, 32(6): 401-404,447. doi: 10.3969/j.issn.1006-0111.2014.06.001
引用本文: 吴金华, 马慧萍, 蒙萍, 贾正平. 脑缺血和再灌注损伤与防治机制的研究进展[J]. 药学实践与服务, 2014, 32(6): 401-404,447. doi: 10.3969/j.issn.1006-0111.2014.06.001
shu
WU Jinhua, MA Huiping, MENG Ping, JIA Zhengping. Mechanisms of damage and treatments of cerebral ischemia and reperfusion[J]. Journal of Pharmaceutical Practice and Service, 2014, 32(6): 401-404,447. doi: 10.3969/j.issn.1006-0111.2014.06.001
Citation: WU Jinhua, MA Huiping, MENG Ping, JIA Zhengping. Mechanisms of damage and treatments of cerebral ischemia and reperfusion[J]. Journal of Pharmaceutical Practice and Service, 2014, 32(6): 401-404,447. doi: 10.3969/j.issn.1006-0111.2014.06.001
shu

    全文HTML

参考文献 (36)

目录

    /

    返回文章
    返回

    版权所有：《药学实践与服务》编辑委员会

    主管、主办: 中国人民解放军海军军医大学地址: 上海市杨浦区国和路325号邮政编码: 200433

    电话: （021）81871324,81871397 E-mail: yxsjzzs@163.com

    网站备案号 沪ICP备05003363号-1

    本系统由 北京仁和汇智信息技术有限公司 开发    百度统计