摘要
目的 观察降钙素基因相关肽 (CGRP)对短暂性脑缺血脑组织神经元凋亡 /死亡的影响 ,探讨其对缺血脑组织的保护作用。方法 应用颈动脉负压分流法制作大鼠短暂性全脑缺血模型 ;于再灌注开始 ,经颈动脉注入CGRP ;应用末端脱氧核苷酸转移酶缺口标记 (TUNEL)法检测神经元凋亡 /死亡。结果 全脑缺血海马CAI区和皮层TUNEL阳性细胞百分率分别为 78.6 0± 4 .82和 5 4 .5 2± 5 .33,显著高于假手术组(2 .4 7± 0 .5 9和 3.4 0± 1.10 ) (P <0 .0 1) ;CGRP组海马和皮层神经细胞凋亡的百分率分别为 5 9.4 2± 3.71和36 .5 7± 5 .32 ,明显低于全脑缺血组 (P <0 .0 1)。结论 CGRP可减少大鼠短暂性全脑缺血脑组织神经元的凋亡 /死亡 ,对缺血神经元具有保护作用。
Objective To observe the effect of calcitonin gene related peptide(CGRP) on neuron apoptosis/death and probe into the protective effect of it on ischemic cerebral tissue.Methods The model of temporary whole cerebral ischemia in rats was induced by means of carotid artery negative pressure shunt(CANPS);CGRP was injected into internal carotid at the beginning of reperfusion.The number of apoptosis/dead neurocyte in brain tissue were detected by method of terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labeling (TUNEL).Results The percentage of TUNEL staining positive cells in hippocampus CAI and cortex in ischemic group were 78.60 ± 4.82 and 54.52 ± 5.33 respectively, much higher than that of in sham group( 2.47 ± 0.59 and 3.40 ± 1.10 )( P < 0.01 );The percentages of TUNEL staining positive cells in hippocampus CAI and cortex in CGRP group were 59.42 ± 3.71 and 36.57 ± 5.32 , much lower than that of in ischemic group ( P < 0.01 ).Conclusion CGRP might reduce apoptosis/death in neuron after temporary whole cerebral ischemia in rats and have protective effect on ischemic neurons.
出处
《卒中与神经疾病》
2002年第6期331-334,共4页
Stroke and Nervous Diseases
基金
辽宁省自然科学基金 (6190 19)
江苏省高校重点实验室开放研究课题 (K2 0 94)资助项目