期刊文献+

一氧化氮和Ca^(2+)含量对缺血再灌注大鼠脑细胞凋亡的影响 被引量:3

Influence of NO and Ca^(2+) Concentration on Cerebral Cell Apoptosis after Cerebral Ischemia Reperfusion
下载PDF
导出
摘要 目的:通过观察脑缺血再灌注时脑组织一氧化氮(NO)和Ca2+含量及脑细胞凋亡的变化,探讨NO、钙对脑细胞凋亡的作用。方法:本实验在建立大鼠急性全脑缺血再灌注损伤模型的基础上,用Green法测定脑组织NO的含量,用原子分光光度仪测定脑组织Ca2+含量,用流式细胞仪检测脑凋亡细胞。结果:脑缺血再灌注12h、24h,NO含量及Ca2+含量均较假手术组增加(P<0.05,P<0.01),脑细胞凋亡数亦增加(P<0.01),且随时间延长进一步增加(P<0.05)。脑缺血再灌注12h、24h时,脑组织Ca2+含量与脑细胞凋亡数呈正相关(P<0.05)。结论:全脑缺血再灌注损伤时发生脑细胞凋亡与脑组织NO、Ca2+含量增高有关。 Objcetive: To investigate the role of NO and calcium on cerebral cell apoptosis after ischemia reperfusion. Method: Use Pulsinelli's methods to create rat model with cerebral ischemia reperfusion injury. The production of NO was measured by Green methods. Atomic absorption spectrophotometer (AAS) was used to analyse calcium concentration, and flow cytomyter(FCM) was used to analyse apoptosis. Results: The production of NO and calcium concentration during ischmia rcperfusion 12,24 hours are higher than shamoperation group(P〈0.05, P〈 0.01 ). At the same time apoptotic cerebral cells number increased with time - dependent manner. Variation of calcium concentration and apoptotic cerebral cells number show a marked positive relationship during ischemia reperfusion 12,24 hours( P 〈 0.05). Conclusion: The cerebral cell apoptosis after ischemia reperfusion relates to the increasing of NO and calcium concentration of brain tissues.
出处 《微循环学杂志》 2005年第3期5-7,F0005,F0007,共5页 Chinese Journal of Microcirculation
基金 湖北省卫生厅基金资助项目(WJ01518)
关键词 脑缺血再灌注损伤模型 CA^2+含量 脑细胞凋亡 一氧化氮 大鼠 全脑缺血再灌注 脑组织NO 损伤过程 Cerebral ischemia and reperfusion Nitric oxide( NO) Calcium Cerebral cell apoptosis Rat
  • 相关文献

参考文献1

二级参考文献10

共引文献6

同被引文献24

  • 1孙耕耘,王应灯.G蛋白偶联受体激酶2参与血小板活化因子致肺微血管内皮细胞损伤的机制[J].中华急诊医学杂志,2004,13(9):602-605. 被引量:10
  • 2郭志凌,赵华月,郑信华.局限缺血-再灌注心肌细胞内钙超负荷发生机制的探讨[J].同济医科大学学报,1995,24(3):198-201. 被引量:9
  • 3Longa EZ, Weinstein PR, Carlson S, et al. Reversible middle cerebral artery occlusion without craniectomy in rats [J]. Stroke, 1989,20(1) :84 - 91.
  • 4Longa EZ,Weinstein PR,Carlson S,et al. Reversible middle cerebral artery occlusion without craniectomy in rats[J]. Stroke, 1989,20( 1 ): 84-91.
  • 5Vannucci RC, Brucklacher RM, Vannucci SJ. In tracellular calcium accumulation during the evolution of hypoxic-ischemic brain damage in the immature rat [ J]. Brain Res Dev Bra in Res, 2001, 126 (1): 117-120.
  • 6Raymoond JR. Multiple mechanisms of receptors G protein signaling specifity [J]. Am J Physiol, 1995, 269 (2) : 141-158.
  • 7Martini, Philip W, Raake J, et al. Targeted Inhibition of Cardiomyocyte Gi Signaling Enhances Susceptibility to Apoptotic Cell Death in Response to Ischemic Stress [ J ]. Circulation, 2008, 117: 1378-1387.
  • 8Mochizuki S, Jiang C. Na/Ca2 exchanger and myocardial ischemia/reperfusion [ J]. Jpn Heart J, 1998, 39 (6) : 707- 714.
  • 9Makrs AR. Intracellular calcium-release channels : regulators of cell life and death [J]. Am J Physiol, 1997, 272 (597) : 113-178.
  • 10Tang XH, Gao J, Fang F, et al. Hepatoprotection of oleanolic acid is related to its inhibition on mitochondrial permeability transition [J]. Am J Chin Med, 2005, 33: 627-637.

引证文献3

二级引证文献10

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