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为探讨巴曲酶对大鼠短暂性脑缺血再灌流损伤引起的细胞凋亡有无抑制作用，参照Ｓｍｉｔｈ等（１９８４）方法，制备大鼠前脑短暂性缺血再灌流模型，采用ＴＵＮＥＬ（脱氧核苷酸转移酶末端介导的ｄＵＴＰ－生物素切口末端标记）法，观察了海马脑区细胞凋亡的特征变化—ＤＮＡ降解片段（凋亡小体）。发现脑缺血１０ｍｉｎ再灌流２４ｈ，海马ＣＡ１区即可见凋亡小体，于再灌流４８ｈ、９６ｈ凋亡小体明显增多。给予巴曲酶（１．６ＢＵ／ｋｇ．ｉｖ）后上述变化被明显逆转。本实验提示巴曲酶对脑缺血再灌流损伤所引起的细胞凋亡有抑制作用。
To investigate whether batroxobin can inhibit the apoptosis induced by transient cerebral ischemia-reperfusion injury in rats, a transient ischemic-reperfusion model of forebrain was established by the method of Smith et al. (1984) Deoxyribonucleotide transferase end-mediated dUTP-biotin nick end labeling) method was used to observe the characteristic changes of apoptosis in the hippocampus-DNA degradation fragments (apoptotic bodies). Apoptotic bodies were found in CA1 area of hippocampus after cerebral ischemia 10 min and reperfusion for 24 h. The number of apoptotic bodies increased significantly at 48 h and 96 h after reperfusion. The above changes were significantly reversed after administration of batroxobin (1.6 BU / kg.iv). This experiment suggests that batroxobin can inhibit the apoptosis induced by cerebral ischemia-reperfusion injury.