期刊文献+

缺血再灌注大鼠脑内MMP-2、MMP-9与血脑屏障的关系 被引量:9

The relationships between MMP-2.MMP-9 and blood-brain barrier in rats with cerebral ischemia and reperfusion
下载PDF
导出
摘要 目的明确脑缺血再灌注后MMP-2、MMP-9与血脑屏障的关系。方法健康雄性SD大鼠54只,线栓法制作大鼠大脑中动脉缺血再灌注模型。应用含明胶的定量酶谱技术检测再灌注3h到7d内MMP-2、MMP-9的表达,用甲酰胺浸泡法检测大鼠脑内EB含量。结果 (1)缺血再灌注24h后,大鼠缺血侧脑内MMP-9表达明显升高,48h到达顶峰,4d后显著下降,7d后水平更低。24h组和48h组与其它各组相比,有显著性差异(P<0.05)。 0MMP-2缺血再灌注48h后明显升高,7d到达高峰,7d组大鼠缺血侧脑内MMP-2水平与3h组和24h组相比,有显著性差别(P<0.01)。(2)再灌注24h大鼠缺血侧脑内EB含量最高,显著高于3h及7d组(P<0.05),但与48h无显著差别(P>0.05)。结论缺血再灌注后出现了MMP-2、MMP-9和血脑屏障的动态变化,血脑屏障损伤与MMP-9 的升高相关,而与MMP-2关系不大。 Objective To investigate the relationships between MMP-2,MMP-9 and blood brain barrier in rats with cerebral isehemia and reperfusion. Methods 54 healthy male SI) rat models with middle cerebral artery occlusion and reperfusion were made by suture method. The expression of MMP-2 and MMP-9 in rat brains over a time course ranging from 3h to 7d after reperfusion was measured by gelatin-containing SDS-PAGE zymography. Brain EB content in rat brains was measured within 7d by formamide extraction method. Results The expression of MMP-9 increased dramatically at 24h and reached the peak at 48h,then decreased at 4d and 7d. MMP 9 activity in 24h and 48h groups showed significant difference compared with all other groups (P〈0.05). The expression of MMP-2 began to increase at 48h and peaked at 7d. Significant difference was seen between 3h,24h and 7d (P〈0. 01). Brain EB content in rats 24h after reperfusion was significantly increased than that of the rats 3h and 7d after reperfusion (P〈0.05),but showed no difference with rats 48h after reperfusion (P〉0. 05). Conclusion There exists dynamic changes of MMP-2 and MMP 9 after cerebral isehemia and reperfusion. Blood-Brain barrier injury was much more likely associated with elevated levels of MMP-9 but not MMP 2.
出处 《中风与神经疾病杂志》 CAS CSCD 北大核心 2006年第2期146-148,共3页 Journal of Apoplexy and Nervous Diseases
关键词 基质金属蛋白酶 再灌注损伤 血脑屏障 脑缺血 Matrix metalloproteinase Reperfusion injury Blood-brain barrier Brain isehemia
  • 相关文献

参考文献10

  • 1Gasche Y,Fujimura M,Morita-Fujimura Y,et al.Early appearance of activated matrix metalloproteinase-9 after focal cerebral ischemia in mice:A possible role in blood-brain barrier dysfunction[J].J of Cerebral Blood Flow and Metabolism,1999,19(9):1020-1028.
  • 2Kondo T,Reaume AG,Huang TT,et al.Reduction of CuZn-superoxide dismutase activity exacerbates neuronal cell injury and edema formation after transient focal cerebral ischemia[J].J Neurosci,1997,17(11):4180-4189.
  • 3Chan PH,Schmidley JW,Fishman RA,et al.Brain injury,edema,and vascular permeability changes induced by oxygen-derived free radicals[J].Neurology,1984,34(3):315-320.
  • 4Mayhan WG,Didion SP.Glutamate-induced disruption of the blood-brain barrier in rats.Role of nitric oxide[J].Stroke,1996,27(5):965-970.
  • 5Rosenberg GA,Estrada EY,Dencoff JE.Matrix metalloproteinases and TIMPs are associated with blood-brain barrier opening after reperfusion in rat brain[J].Stroke,1998,29(10):2189-2195.
  • 6Birkedal HH.Role of cytokines and inflammatory mediators in tissue destruction[J].J Periodontal Res,1993,28(2):500-510.
  • 7Tomasek JJ,Halliday NL,Updike DL,et al.Gelatinase A activation is regulated by the organization of the polymerized actin cytoskeleton[J].J Biol Chem,1997,272 (11):7482-7487.
  • 8Asahi M,Wang X,Mori T,et al.Effects of matrix metalloproteinase-9 gene knock-out on the proteolysis of blood-brain barrier and white matter components after cerebral ischemia[J].J Neurosci,2001,21(19):7724-7732.
  • 9Tsuji K,Aoki T,Tejima E,et al.Tissue plasminogen activator promotes matrix metalloproteinase-9 upregulation after focal cerebral ischemia[J].Stroke,2005,36(9):1954-1959.
  • 10Romanic AM,White RF,Arleth AJ,et al.Matrix metalloproteinase expression increases after cerebral focal ischemia in rats.Inhibition of matrix metallopoteinase-9 reduces infarct size[J].Stroke,1998,29 (10):1020-1030.

同被引文献65

引证文献9

二级引证文献63

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部