首页 | 本学科首页   官方微博 | 高级检索  
     

局灶性脑梗死后半暗带区皮层血流量与神经细胞凋亡的实验研究
引用本文:王贤军,夏青,蔡洪信,夏作理. 局灶性脑梗死后半暗带区皮层血流量与神经细胞凋亡的实验研究[J]. 中国病理生理杂志, 2006, 22(5): 968-971. DOI: 1000-4718
作者姓名:王贤军  夏青  蔡洪信  夏作理
作者单位:1泰山医学院脑微循环研究所, 山东 泰安 271000; 2 北京大学药学院化学生物系, 北京 100083
基金项目:山东省自然科学基金资助项目
摘    要:目的:研究大鼠局灶性脑梗死后半暗带区皮层血流量及神经细胞凋亡。 方法: 光化学法诱导大鼠局灶性脑梗死模型,应用激光多普勒微循环测量仪检测局灶性脑梗死后各时间点坏死区和半暗带皮层血流量;TdT-介导dUTP-生物缺口末端标记(TUNEL)法检测凋亡细胞。 结果: 脑梗死后坏死区皮层血流量呈波浪样改变,3 h降至最低,为正常血流量的9.36%±1.72%,6h后回升,12 h达高峰,为正常31.18%±1.44%,24-48 h血流量再度下降,与3 h相比无显著差异(P>0.05)。半暗带皮层血流量6 h降至最低,为正常皮层血流量的30.88%±7.11%,9-48 h上升,至48 h血流恢复至正常91.90%±4.56%,与其它组差异显著 (P<0.05)。TUNEL结果显示,局灶性脑梗死组 6 h 开始出现凋亡细胞,主要集中于半暗带区,呈半球状向四周放射样扩展,随梗死时间的延长凋亡细胞逐渐增多,梗死48 h后凋亡细胞达峰值。 结论: 局灶性脑梗死后半暗带区皮层血流量与神经细胞凋亡具有明显的关系,其血流量的恢复引起的再灌注损伤最终导致了迟发性神经细胞凋亡。

关 键 词:神经元  细胞凋亡  大脑梗死    
文章编号:1000-4718(2006)05-0968-04
收稿时间:2004-09-09
修稿时间:2004-09-092004-11-25

Relation between rCBF and neuronal apoptosis in penumbra following focal cerebral infarction
WANG Xian-jun,XIA Qing,CAI Hong-xin,XIA Zuo-li. Relation between rCBF and neuronal apoptosis in penumbra following focal cerebral infarction[J]. Chinese Journal of Pathophysiology, 2006, 22(5): 968-971. DOI: 1000-4718
Authors:WANG Xian-jun  XIA Qing  CAI Hong-xin  XIA Zuo-li
Affiliation:1Institute of Cerebral Microcirculatin, Taishan Medical College, Taian 271000, China; 2 Department of Chemical Biology, School of Pharmaceutical Sciences, Peking University Health Science Center, Beijing 100083, China
Abstract:AIM: To study regional cerebral blood flow (rCBF) and neuronal apoptosis in penumbra following focal cerebral infarction in rats. METHODS: To establish the model of focal cerebral infarction based on the principle of photochemical initiation of thrombosis. Laser Doppler flowmetry was used to measure rCBF in ischemic core and penumbra. The numbers and anatomic distribution of apoptosis cells were examined in situ histologically with terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-fluorescein nick end-labeling (TUNEL) assay in adjacent sections. RESULTS: rCBF in penumbra decreased to the minimum at 6 h in which it was 30.88%±7.11% of normal. From 9 h to 48 h, rCBF in penumbra increased gradually. At 48 h, 91.90%±4.56% of normal cerebral blood flow was recovered which was significant differences than others. Terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-fluorescein nick end-labeling (TUNEL) assay demonstrated that TUNEL-positive cells occurred at 6 h and were expending in a radial fashion only in penumbra. The numbers of apoptosis cells were progressively increased with time and to the maximum in penumbra after 48 h following focal cerebral infarction. CONCLUSION: There were delayed neuronal apoptosis following focal cerebral infarction. The mechanism may be related to ischemia-reperfusion injury induced by the recovery of rCBF in penumbra.
Keywords:Neurons  Apoptosis  Cerebral infarction  Light
本文献已被 CNKI 万方数据 等数据库收录!
点击此处可从《中国病理生理杂志》浏览原始摘要信息
点击此处可从《中国病理生理杂志》下载全文
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号