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目的：细胞凋亡是细胞死亡的一种形式，对缺血后梗塞灶的发生、发展有一定的作用。故测定缺血脑区出现ＤＮＡ片断化的凋亡细胞数量变化及在缺血脑区的分布状况，以了解脑缺血的病理生理及寻求防治措施。方法：利用线栓法制成大脑中动脉缺血动物模型，测定脑组织ＳＯＤ、ＬＰＯ含量变化及凋亡细胞的密度变化；利用脱氧核苷酸末端转移酶介导的ｄＵＴＰ－荧光素缺口末端标记技术（ＴＵＮＥＬ）原位检测细胞核内的特征性ＤＮＡ片断，具特异性，在光镜下即可被辨认。结果：随缺血时间的持续，缺血侧凋亡细胞的密度增加，脑组织ＳＯＤ含量下降、ＬＰＯ上升；同一缺血时刻下视前区与纹状体的细胞凋亡密度高于皮层，即凋亡主要发生在缺血中心区近中线侧区域，提示“半暗带”的细胞死亡可能以凋亡形式为主，也可能是缺血后自由基介导的凋亡增加。结论：“半暗带”内细胞以凋亡形式死亡为主，对缺血灶不可逆性改变有重要作用。
Aim: Apoptosis is a form of cell death that has some effect on the occurrence and development of ischemic infarction. Therefore, the determination of ischemic brain areas appeared DNA fragmentation of apoptotic cells and changes in the distribution of ischemic brain regions in order to understand the pathophysiology of cerebral ischemia and seek prevention and treatment measures. Methods: The animal models of middle cerebral artery occlusion (MCAO) were established by the method of thread occlusion. The changes of SOD and LPO contents and the density changes of apoptotic cells were determined. The expression of dUTP-fluorescein nick end-labeling (TUNEL) In situ detection of characteristic DNA fragments in the nucleus is specific and can be identified under light microscopy. Results: With the prolongation of ischemia time, the density of ischemic apoptotic cells increased, the content of SOD in brain tissue decreased and LPO increased. The apoptotic density of preoptic area and striatum under the same ischemia was higher than that of cortex Apoptosis occurred mainly in the midline region of the ischemic center, suggesting that the “penumbra” cell death may be mainly in the form of apoptosis, and may also be mediated by free radical-mediated apoptosis after ischemia. Conclusion: The death of the cells in the penumbra is mainly death, which plays an important role in the irreversible changes of the ischemic focus.