大鼠慢性局灶脑缺血区CD8抗原表达的免疫组织化学研究

本文目的在于探查免疫分子 CD8抗原在脑缺血区表达的状况 ,进而探讨免疫因素与慢性局灶脑缺血的病理联系。采用大脑中动脉阻塞的局灶脑缺血模型和免疫组织化学 ABC方法观察 3 6只成年雄性 SD大鼠脑缺血区 CD8抗原表达的细胞种类、分布形式和表达时程。结果证明 :慢性局灶脑缺血诱导脑缺血区 CD8抗原表达 ,其阳性细胞呈无突起的圆形和分支状二类。圆形细胞在脑缺血 3 d时 ,其数量显著增加 (P<0 .0 5 ) ,位于大脑皮质梗塞灶的边缘 ,阳性细胞于脑缺血 1周达到高峰 (P<0 .0 1) ,此时 ,大部分阳性细胞已迁移到梗塞灶中央区并显示为大小和形状不同的无突起的细胞。分支状的 CD8阳性细胞出现在大脑皮质梗塞灶周围和缺血侧尾壳核 ,其数量在脑缺血 3 d显著增加 (P<0 .0 5 ) ,于脑缺血 1周 (尾壳核 )和 2周 (大脑皮质 )时达到高峰 (P<0 .0 1) ,随后缓慢下降 ,分支状的 CD8阳性细胞主要分布于大脑皮质梗塞灶的“半影区”和尾壳核的背外侧区。结果表明 :慢性局灶脑缺血诱导 CD8阳性 T淋巴细胞在脑缺血区浸润以及小胶质细胞的反应和激活 ,提示免疫因素与慢性局灶脑缺血有关联

IMMUNOHISTOCHEMICAL EXPLORATION OF CD8 ANTIGEN EXPRESSION IN THE RAT BRAIN OF CHRONIC FOCAL ISCHEMIA

To explore the expression profile of immunomolecule CD8 antigens in the ischemic rat brains and to inquire into with pathological relationship of immune factors with the chronic focal cerebral ischemia, the cellular type and distribution pattern as well as time course of CD8 antigen expression were examined immunohistochemically in the 36 SD rat ischemic brains with the model of middle cerebral artery occlusion. The results verified (1) that ischemia-induced CD8 positive cells showed both round, lacked process and ramified forms, and the round CD8 positive cells increased in number (P<0.05) and were present in the periphery of cortical ischemic foci at 3 d postischemia, whose number increased further and peaked in number (P<0.01) as well as were localized in the ischemic cerebral core at 1 w postischemia, thereafter, the CD8 positive cells with different size and shape decreased progressively in number, (2) that the ramified CD8 positive cells were present both in the periphery of ischemic cortex and in the ischemic caudoputamen. The number increased (P<0.05) at 3 d postischemia, and peaked (P<0.01) at 1 w postischemia (ischemic caudoputamen) and 2 w positischemia (ischemic cortex), and then, it decreased slowly. The ramified CD8 positive cells were localized both in the penumbra of ischemic cortex and in the ischemic lateral caudoputamen. These results showed that chronic focal ischemia induced both the infiltration of CD8 positive T lymphocytes, and the microglial reaction and activation, which indicated that immune factors participated in the pathological mechanism of chronic focal cerebral ischemia.