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

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

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
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

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
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

  • 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。
  • [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] 竺东杰, 贺新征, 邹杰, 余史丹, 李红霞.  雷公藤甲素对大鼠脑缺血再灌注损伤的影响及机制研究 . 药学实践与服务, 2024, 42(): 1-6. doi: 10.12206/j.issn.2097-2024.202311021
    [2] 刘景雪, 何瑞华, 陶霞, 黄瑾.  参麻颈复方对脑缺血损伤小鼠的脑保护作用及其机制研究 . 药学实践与服务, 2023, 41(11): 666-671, 685. doi: 10.12206/j.issn.2097-2024.202208066
    [3] 李莉, 冯晶晶, 李铁军, 章越凡.  复元醒脑汤对大鼠局灶性脑缺血再灌注损伤的保护作用研究 . 药学实践与服务, 2018, 36(1): 34-39. doi: 10.3969/j.issn.1006-0111.2018.01.007
    [4] 冯晶晶, 李铁军, 章越凡.  丹参酮ⅡA对脑缺血后炎性反应影响机制的研究进展 . 药学实践与服务, 2018, 36(2): 108-111. doi: 10.3969/j.issn.1006-0111.2018.02.003
    [5] 高越, 陈安妮, 赵亚红, 薛丹, 安泳潼, 柴逸峰, 张海.  养心氏片防治慢性缺血性心力衰竭及急性心肌缺血再灌注损伤的实验研究 . 药学实践与服务, 2016, 34(5): 403-407,415. doi: 10.3969/j.issn.1006-0111.2016.05.006
    [6] 程晶晶, 刘谋治, 李洪娇, 阎澜, 姜远英, 颜天华.  新化合物TG6对心肌缺血/再灌注损伤的影响及机制研究 . 药学实践与服务, 2014, 32(6): 440-443. doi: 10.3969/j.issn.1006-0111.2014.06.010
    [7] 邵尉, 舒丽芯, 李捷玮.  中、美军队战伤感染防治用药比较 . 药学实践与服务, 2014, 32(1): 71-73. doi: 10.3969/j.issn.1006-0111.2014.01.020
    [8] 林峰, 周志军, 张晨虹, 刘芳, 郭闻渊, 魏若菡, 陈慧.  用乌司他丁抑制炎症反应减轻大鼠移植肝再灌注损伤的实验研究 . 药学实践与服务, 2014, 32(2): 110-113,127. doi: 10.3969/j.issn.1006-0111.2014.02.009
    [9] 杨宏, 倪敏, 赵心彬, 陶霞.  辐射致组织损伤凋亡机制的研究概况 . 药学实践与服务, 2014, 32(2): 96-97,149. doi: 10.3969/j.issn.1006-0111.2014.02.005
    [10] 娄月芬, 李盈, 胡滨.  豨莶草总黄酮对大鼠脑缺血损伤的保护作用及其作用机制研究 . 药学实践与服务, 2013, 31(1): 42-44. doi: 10.3969/j.issn.1006-0111.2013.01.012
    [11] 倪敏, 沈甫明.  肝脏缺血再灌注损伤发生机制及药物干预研究进展 . 药学实践与服务, 2011, 29(3): 179-180,211.
    [12] 田谋利, 李铁军, 刘虎, 邹最, 石学银.  尿苷三磷酸对大鼠脑缺血再灌注损伤保护作用的机制初探 . 药学实践与服务, 2010, 28(3): 181-183,234.
    [13] 曹国建, 唐志华, 丁洁卫, 陈梅莉.  大环内酯类抗生素的心脏毒性及防治 . 药学实践与服务, 2002, (5): 271-272.
    [14] 胡佳乐, 张川, 苏定冯.  G-CSF减轻大鼠下肢缺血再灌注致肺功能损伤的实验研究 . 药学实践与服务, 2001, (1): 14-16.
    [15] 卫洪昌, 王秀薇, 吕嵘, 程金波, 朱晓梅, 吴倩, 章忱.  益心口服液药物预处理对大鼠心肌缺血再灌注损伤的影响 . 药学实践与服务, 2001, (3): 157-159.
    [16] 胡佳乐, 李伟, 沈甫明.  腺苷预适应对缺血再灌注损伤的保护作用 . 药学实践与服务, 2001, (4): 206-208,205.
    [17] 孙平龙, 朱晓梅, 卫洪昌.  徐长卿内关穴位注射对大鼠心肌缺血再灌注损伤的影响 . 药学实践与服务, 2000, (4): 212-215.
    [18] 刘元生, 孙慧宽, 邱能庸, 张艳萍.  吲哒帕胺、维拉帕米对兔心肌再灌注损伤保护机制的探讨 . 药学实践与服务, 1998, (6): 322-325.
    [19] 李飒, 李万亥, 陶学斌, 陈东明, 陈洁.  二乙基二硫代氨基甲酸钠对沙土鼠脑缺血再灌注损伤的保护作用 . 药学实践与服务, 1995, (3): 136-139.
    [20] 陶学斌, 李万亥.  钙超载与心肌缺血再灌注损伤 . 药学实践与服务, 1993, (4): 242-244.
  • 加载中
计量
  • 文章访问数:  2819
  • HTML全文浏览量:  391
  • PDF下载量:  135
  • 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
    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).

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
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
参考文献 (36)

目录

    /

    返回文章
    返回