摘要
目的研究异亚丙基莽草酸(ISA)对大脑中动脉缺血再灌注大鼠的影响及初步作用机制。方法栓线法建立大鼠大脑中动脉缺血再灌注模型,缺血3h,再灌注21h后以TTC染色法测定脑梗死范围,比色法测定脑组织匀浆中髓过氧化物酶(MPO)活性,ELISA法测定匀浆中IL-1β,IL-8,TNF-α含量。结果ISA 200,100 mg·kg-1可明显减少模型大鼠的脑梗死范围,降低脑组织匀浆MPO活性以及IL-1β,IL-8,TNF-α的水平。结论ISA对局灶性脑缺血再灌注损伤具有明显的阻抑作用,其作用机制与抗炎症反应有关。
Abstract
OBJECTIVE To study the effects of 3,4-oxo-isopropylidene shikimia acid(ISA) on the inflammatory reaction after cerebral ischemia and reperfusion in tMCAO(transient middle cerebral artery occlusion) rats, and its probable mechanism.METHODS The rats were subjected to MCAO for 3 h. After 21 h of reperfusion, TTC staining of brains was made to determine the size of cerebral infarction. The contents of IL-8,TNF-α, IL-1β and MPO in brain tissue were assayed. RESULTS After tMCAO, the vehicle group manifested the size of cerebral infarction as well as the content of TNF-α,IL-1β,IL-8 and MPO raised vs ISA group, ASA group and sham group. Above indicators were decreased significantly(P< 0.05 or 0.01 )in ISA 200,100 mg·kg-1 and ASA 50 mg·kg-1. CONCLUSION ISA can relieve the inflammatory reaction, namely leukocytic infiltrate and expression of inflammatory cytokine in brain tissue after cerebral ischemia and reperfusion, which may be an important mechanism for its resisting ischemic and reperfusion injury.
关键词
异亚丙基莽草酸 /
大脑中动脉 /
脑缺血再灌注 /
炎症 /
髓过氧化物酶 /
细胞因子
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Key words
3 /
4-oxo-isopropylidene shikimic acid (ISA) /
middle cerebral artery /
cerebral ischemia and reperfusion /
inflammation /
myeloperoxidase(MPO) /
cytokine
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孙文燕;孙建宁;刘振权;黄贱英;张文博.
异亚丙基莽草酸抗大鼠脑缺血再灌注损伤的炎症机制初探[J]. 中国药学杂志, 2005, 39(09): 678-680
SUN Wen-yn;SUN Jin-ning;LIU Zhen-qun;HUNG Jin-ying;ZHNG Wen-o.
Effects of 3,4-oxo-isopropylidene shikimic acid (ISA) on the inflammatory reaction in rats subjected to middle cerebral artery ischemia and reperfusion and its probable mechanism [J]. Chinese Pharmaceutical Journal, 2005, 39(09): 678-680
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参考文献
[1]王宏涛, 靳洪涛, 孙建宁, 等. 异亚丙基莽草酸抗血栓作用的实验研究[J]. 药学学报,2002, 37(4):245.
[2]王宏涛,孙建宁,徐秋萍,等. 异亚丙基莽草酸对大脑中动脉栓塞大鼠脑含水量和能量代谢的影响[J]. 中国药理学与毒理学杂志,2002,16(4):270.
[3]Koizumi J, Yoshida Y, Nakazawa T,et al.Experimental studies of ischemia brain edema,Ⅰ: A new experimental model of cerebral embolism in rats in which recirculation can be introduced in the ischemic area[J].Jpn J Stroke,1986,8:1.
[4]Nagasawa H, Kogure K. Correlation between cerebral blood flow and histologic changes in a new rat model of middle cerebral artery occlusion[J].Stroke,1989,20(8):1037.
[5]Zhang Z, Chopp M, Goussev A, et al. Cerebral vessels express interleukin-1 beta after focal cerebral ischemia[J].Brain Res,1998,784(1-2):210.
[6]Stroemer RP, Rothwell NJ. Exacerbation of ischemic brain damage by localized striatal injection of interleukin-1beta in the rat[J].J Cereb Blood Flow Metab,1998,18(8):833.
[7]Yamasaki Y, Matsuura N, Shozuhara H, et al. Interleukin-1 as a pathogenetic mediator of ischemic brain damage in rats[J].Stroke,1995,26(4): 676.
[8]Kostulas N, Kivisakk P, Huang Y, et al. Ischemic stroke is associated with a systemic increase of blood mononuclear cells expressing interleukin-8 mRNA[J].Stroke,1998,29(2):462.
[9]Zhai QH,Furrell N,Chen FJ.Gene expression of IL-10 in relationship to TNF-alpha, IL-1beta and IL-2 in the rat brain following middle cerebral artery occlusion[J].J Neurol Sci,1997,152:119.
[10]Matsuo Y, Ondera H, ShigaY.Correlation between myeloperxidase quantified neutrophil accumulation and ischemic brain injury in the rat: effects of neutrophil depletion[J].Stroke,1994,25 (7):1469.
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脚注
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基金
国家科技部“十五”科技攻关项目(2001BA701A07-14)
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