大鼠脑缺血后胼胝体少突胶质细胞变化的特征

The change of oligodendrocyte in rats following cerebral ischemia

目的观察脑缺血大鼠胼胝体少突胶质谱系细胞的动态变化规律。方法采用4-VO脑缺血模型,随机分为2d、4d、7d、14d和28d 5个时间点及假手术组,每组8只;用组织芯片免疫组织化学检测胼胝体A2B5、O4、CNPase蛋白表达变化。结果 (1)CNPase阳性细胞于脑缺血后有不同程度减少,2d即明显减少,7d时减少到最低,14d时回升,28d时恢复至假手术组水平;与假手术组比较,脑缺血后2d、4d、7d有显著差异(P<0.05)。(2)O4阳性细胞数于脑缺血后2d时显著减少,4d时回升,28d时恢复至假手术组水平;与假手术组比较,2d、4d有显著差异(P<0.05)。(3)A2B5阳性细胞于脑缺血后随着再灌注时间延长而增加,2d时即已增多,持续至28d时达到高峰;与假手术组比较,7d、14d、28d有显著差异(P<0.05)。结论脑缺血后OPC反应性增生,未成熟和成熟OLG减少,以未成熟OLG为著;提示未成熟OLG对缺血有易损性,而OPC有耐受性。

Objective To investigate the characteristic change of the oligodendrocyte lineage cells in the corpus cal- losum following cerebral ischemia after four-vessel occlusion （4-VO）. Methods The rat model of whole-brain ischemia was established by exposing the brain of healthy adult Sprague-Dawley rat to four-vessel occlusion（4-VO）. The expression of A2B5,O4 and CNPase in the corpus callosum of rat brain was measured by tissue microarray technology and immunohistochemistry at the time-points of 2d ,4d ,7d, 14d and 28d after 4-VO. Results （ 1 ） The number of CNPase-positive ceils decreased on 2d just after 4-VO and reached peak on 7d. Then it dropped gradually on 14d and returned to the control level on 28d. Compared to sham operated group,the number of CNPase-positive cells decreased significantly on 2d,4d and 7d（P 〈 0.05 ）. （ 2 ） O4-positive cells decreased significantly on 2d. Then the number dropped gradually on 4d and got back to the control level on 28d. Compared with sham operated group, the number of O4-positive cells decreased significantly on 2d and 4d（P 〈 0.05 ）. （3）A2B5-positive cells increased time-dependently after 4-VO. It started to increase on 2d,but there was no significant difference compared with that of the sham operated group. A2B5-positive cells increased significantly from 7d until 28d. Compared with sham operated group, there was a significant difference on 7d, 14d and 28d （ P 〈 0.05 ）. Conclusions OPCs were upregulated and proliferated after cerebral ischemia. The early disappearance of mature oligodendrocyte was followed by activation of the OPC, suggesting that the early oligodendrocyte progenitor were highly resistant to ischemia but the late oligodendroeyte progenitor was highly susceptible.