期刊文献+

实验性大鼠脑动脉瘤形成过程中MMP-2、MMP-9表达的动态变化 被引量:2

Expression of matrix metalloproteinase 2 and 9 in hypertension-induced intracranial aneurysm in rats
下载PDF
导出
摘要 目的探讨实验性大鼠动脉瘤形成过程中基质金属蛋白酶2(MMP-2)、基质金属蛋白酶9(MMP-9)的表达规律。方法制作肾性高血压大鼠脑动脉瘤模型,通过免疫组化在蛋白水平系统动态观察肾性高血压大鼠脑动脉瘤形成过程中MMP-2、MMP-9表达的变化。结果实验组在术后1 w脑动脉壁即可见MMP-2、MMP-9表达增加,随着术后时间的推移和大鼠血压的增高,其表达也迅速增加,术后1个月基本达最高峰并一直持续至4个月,其中MMP-9较正常状态的增加比MMP-2的表达增加更为显著。对照组脑动脉壁MMP-2、MMP-9也有微弱表达,且MMP-2表达较MMP-9略强。结论脑动脉壁MMP-9、MMP-2特别是MMP-9的过度表达导致的脑动脉壁胶原纤维及内弹力层破坏是脑动脉瘤形成的主要原因之一。 Objective To investigate the expression pattern of matrix metalloproteinase-2 (MMP-2), matrix metaUoproteinase-9 (MMP-9) in the process of aneurysm formation in rats. 1Vleflaods A rat model of cerebral anettrysm was established. The dynamic changes of MMP-2 and MMP-9 expressions were examined by immtmohistochemistry at the level of protein activity in the process of aneurysm formation. Results In experimental group, with the development of hypertension, the expressions of MMP-2 and MMP-9 were increased one week after operation, peaked at first month and lasted until 4 months after operation. The expression of MMP-9 was increased more remarkably than that of MMP-2. Weak staining of MMP-2 and MMP-9 was observed in the cerebral artery, and the expression of MMP-2 was little higher than that of MMP-9. Conclusion The over-expressions of MMP-2 and MMP-9 in artery which result in the wall destruction of collagen and internal elastic lamina of cerebral artery are the main cause of the aneurysm formation.
出处 《中华神经外科疾病研究杂志》 CAS 2013年第3期197-200,共4页 Chinese Journal of Neurosurgical Disease Research
关键词 颅内动脉瘤 基质金属蛋白酶2 基质金属蛋白酶9 Intracranial aneurysm MMP-2 MMP-9
  • 相关文献

参考文献20

二级参考文献43

  • 1赵继宗,王忠诚,孙异临,王硕,高鲜红,赵通印,曲宝清.颅内囊性动脉瘤临床病理研究[J].中华神经外科杂志,1996,12(4):234-237. 被引量:6
  • 2[1]Cohen JR, Mandell C, Margolis I, et al. Altered aortic protease and antiprotease activity in patients with ruptured abdominal aortic aneurysms[J]. Surg Gynecol Obstet, 1987,164(4) :355 - 358.
  • 3[2]Stehbens WE. Pathology and pathogenesis of intracranial berry aneurysms[J]. Neurol Res, 1990,12(1) :29- 34.
  • 4[3]Kosierkiewicz TA, Factor SM, Dickson DW. Immunocytochemical studies of atherosclerotic leisions of cerebral berry aneurysms[J]. J Neuropathol Exp Neurol, 1994,53(4) :399 - 406.
  • 5[4]Brown PD, Levy AT, Margulies IM, et al. Independent expression and cellular processing of Mr 72000 type Ⅳ collagenase and interstitial collagenase in human tumorigenic cell lines[J]. Cancer Res, 1990,50(19) :6184 - 6191.
  • 6[5]Davies MJ, Richardson PD, Woolf N, et al. Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid , macrophage , and smooth muscle cell content[J]. Br Heart J, 1993,69(5):377-381.
  • 7[6]Galis ZS, Sukhova GK, Lark MW, et al. Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques[J]. J Clin Invest, 1994,94(6):2394-2503.
  • 8[7]Schievink WI, Prakash UB, Piepgras DG, et al. Alpha 1-antitrypsin deficiency in intracranial aneurysms and cervical artery dissection[J].Lancet, 1994,343 (8895) :452 - 453.
  • 9[8]Schievink WI, Katzmann JA, Piepgras DG, et al. Alpha 1-antitrypsin phenotypes among patients with intracranial aneurysms[J]. J Neurosurg, 1996,84(5) :781 - 784.
  • 10[9]Connolly ES, Fiore AJ, Winfree CJ, et al. Elastin degradation in the superficial temporal arteries of patients with intracranial aneurysms reflects changes in plasma elastase[J]. Neurosurgery, 1997,40(5): 903-909.

共引文献530

同被引文献110

引证文献2

二级引证文献3

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