期刊文献+

灯盏花素对大鼠脑缺血后细胞间粘附分子-1及其mRNA表达的影响 被引量:16

Effect of erigeron on intercellular adhesion molecule-1 and its mRNA expression during cerebral ischemia and reperfusion in rats
下载PDF
导出
摘要 目的灯盏花素对大鼠脑缺血后细胞间粘附分子-1(ICAM-1)及其mRNA表达的影响。方法复制大鼠大脑中动脉闭塞/再灌注模型,应用RT-PCR及免疫组织化学的方法,观察各组大鼠脑缺血后细胞间粘附分子-1mRNA及其蛋白的表达。结果ICAM-1在假手术组大鼠脑组织呈低表达;单纯缺血组(缺血90min)ICAM-1表达上调(P<005);缺血再灌注组(缺血90min再灌24h)脑组织ICAM-1表达显著高于假手术组和单纯缺血组(P<001);灯盏花素治疗组于相同时限ICAM-1表达与单纯缺血、缺血再灌注组相比显著下调(P<001)。大鼠脑组织ICAM-1mRNA在假手术组呈低表达;单纯缺血组ICAM-1mRNA水平显著上调(P<001);药物治疗组于相同时限ICAM-1mRNA水平显著低于单纯缺血组及缺血再灌注组(P<001)。结论灯盏花素下调细胞间粘附分子-1mRNA及其蛋白的表达,减轻缺血后再灌注损伤,从而发挥脑保护作用。 AIM: To investigate the effect of erigeron on intercellular adhesion molecule-1 (ICAM-1) and mRNA expression during cerebral ischemia/reperfusion. METHODS: The rat models of middle cerebral artery (MCA) focal cerebral ischemic reperfusion were established with the suture method in the study. The ICAM-1 mRNA and protein expression were measured by RT-PCR and immunohistochemistry techniques, respectively. RESULTS: By down-regulating the expression of ICAM-1 protein and mRNA and alleviating inflammation in cerebral ischemic region, erigeron exerted a protective effect in cerebral ischemia and reperfusion. CONCLUSION: The results suggest that erigeron protects the brain against cerebral ischemia and reperfusion injury via inhibiting ICAM-1 expression. [
出处 《中国病理生理杂志》 CAS CSCD 北大核心 2004年第12期2287-2290,共4页 Chinese Journal of Pathophysiology
关键词 灯盏花素 脑缺血 细胞间粘附分子1 Erigeron Brain ischemia Intercellular adhesion molecule-1
  • 相关文献

参考文献9

  • 1Longa EZ, Weinstein PR, Carlson S, et al. Reversible middle cerebral artery occlusion without craniectomy in rats[J]. Stroke, 1989, 20(1):84-91.
  • 2Kita Y, Takashi T, Iigo Y, et al. Sequence and expression of rat ICAM-1[J]. Biochim Biophys Acta, 1992, 1131(1):108-110.
  • 3Ikeda K, Wakahara T, Wang YQ, et al. In vitro migratory potential of rat quiescent hepatic stellate cells and its augmentation by cell activation[J]. Hepatology, 1999, 29(6):1760-1767.
  • 4Shyu KG, Chang H, Lin CC. Serum levels of intercellular adhesion molecule-1 and E-selectin in patients with acute ischemic stroke[J]. J Neurol, 1997, 244(2):90-93.
  • 5Zhang RL, Chopp M, Li Y, et al. Anti-ICAM-1 antibody reduces ischemic cell damage after transient middle cerebral artery occlusion in the rat[J]. Neurology, 1994, 44(9): 1747-1751.
  • 6Nishizuka Y. Studies and perspectives of protein kinase C[J]. Science, 1986, 233(4761): 305-312.
  • 7Chen KN, Dong WW. The role of PKC in the progress of ischemic neuronal injury:approach to the mechanism[J]. J Neurochem, 1996, 67(Suppl): S64-S65.
  • 8Di-Capua N, Sperling O, Zoref-Shani E. Protein kinase C-epsilon is involved in the adenosine-activated signal transduction pathway conferring protection against ischemia-reperfusion injury in primary rat neuronal cultures[J]. J Neurochem, 2003, 84(2):409-
  • 9Defazio G, Nico B, Trojano M, et al. Inhibition of protein kinase C counteracts TNF alpha-induced intercellular adhesion molecule 1 expression and fluid phase endocytosis on brain microvascular endothelial cells[J]. Brain Res, 2000, 863(1-2): 245-248.

同被引文献220

引证文献16

二级引证文献147

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