光化学法脑缺血后细胞凋亡及其相关基因bcl-2表达的变化

采用ＴＵＮＥＬ染色及免疫组织化学技术对光化学法脑缺血后细胞凋亡及其相关基因ｂｃｌ－２表达的变化进行了研究。结果发现，缺血后１２ｈ，损伤侧皮层缺血区内凋亡细胞数及ｂｃｌ－２免疫反应阳性细胞数明显增加，一直持续至缺血后７２ｈ；并呈现下列时程变化：在缺血后３ｈ每张切片上几乎无凋亡细胞出现，以后逐渐增加，缺血后１２ｈ达到峰值，缺血后２４ｈ和缺血后７２ｈ逐渐减少，但仍高于假手术组水平。凋亡相关基因ｂｃｌ－２的表达在缺血后３ｈ以前不明显，缺血后１２ｈ逐渐增加，缺血后２４ｈ最多，以后逐渐下降。上述结果提示，缺血后凋亡细胞的时程变化可能与缺血后梗塞灶的发生和发展有关，而ｂｃｌ－２表达的变化可能与抑制细胞凋亡、发挥内源性细胞保护作用有关。

CHANGES OF APOPTOSIS AND APOPTOSIS ASSOCIATED GENE BCL 2 EXPRESSION AFTER PHOTOCHEMICALLY INDUCED CEREBRAL ISCHEMIA IN RATS

In order to elucidate apoptosis in pathogenesis of the photochemically induced ischemic brain damage, the changes of apoptosis and apoptosis related gene bcl 2 expression were studied by means of TUNEL staining and immunohistochemical methods. The rats were divided to sham, 3h, 12h, 24h, 72 groups following cerebral ischemia. Our observation indicated that the numbers of apoptotic cells and bcl 2 immunoreactive positive cells in ischemic area iplateral to irradiated side increased apparently at 12h postischemia and persisted to 72h. Almost to aoptotic cells per section were observed at 3h post ischemia, then it increased gradually, peaked at 12h, and declined at 24h to 72h post lesion. Meanwhile, expression of bcl 2 was not found before 3h post ischemia, and it appeared at 12h, attained the peak at 24h and then decreased. The results suggest that the postischemic time course alteration of apoptotic cells may be associated with the evolution of infarcted area, and temporal changes of bcl 2 expression possibly contribute to inhibiting apoptosis or playing a protective role in cell death induced by ischemic event.