摘要
目的观察慢性脑灌流不足(chronic cerebral hypoperfusion,CCH)老年大鼠脑组织Caspr2表达的变化。方法建立老年大鼠CCH模型,采用免疫荧光组织化学与Western blot法,对大鼠CCH后2周及1、3个月脑组织Caspr2的表达变化进行组织定位与半定量分析。结果脑内Caspr2主要表达于皮质下白质,特别是胼胝体等神经纤维束密集区域,皮质表达较弱;CCH后Caspr2表达数量及强度与对照组相比显著下降,且其定位模式在白质纤维结构中出现分布紊乱;CCH后2周及1、3个月时其表达与对照组比较差异有统计学意义(P<0.05)。结论慢性缺血缺氧导致Caspr2表达显著降低与定位改变,可能是白质结构损害及相关功能减退的重要环节和分子基础。
Objective To investigate the effect of chronic cerebral hypoperfusion （CCH） on the expression of caspr2 in brain tissue in aged rats. Methods The changes in caspr2 expression were examined qualitatively and quantitatively by immunofluorescence staining and Western blotting respectively, in 2 weeks, 1 month and 3 months after establishment of CCH model in cerebral tissue in aged rats. Results The caspr2 immunoreactivity was mainly distributed in the white matter, especially in the bundle nerve fibers. As compared with the normal aged rats, the caspr2 expression significantly decreased after CCH （ F = 24. 852, P = 0. 020; F = 10. 151, P = 0. 015;F^47. 215,P=0. 000）. Its distribution also changed markedly and showed a confusion pattern in the corpus callosum. Conclusions CCH causes an evident decline in the expression of caspr2 and spatial changes as well. It might be a molecular basis and key link for the white matter injury and the cognitive degeneration.
出处
《中国神经免疫学和神经病学杂志》
CAS
2007年第2期87-89,I0002,共4页
Chinese Journal of Neuroimmunology and Neurology
基金
第三军医大学留学回国人员科研启动基金资助项目(2004D115)
