巴曲酶对大鼠脑缺血再灌流损伤保护作用机理的研究  

Study on the mechanisms of the protective effect of batroxobin on cerebral ischemia reperfusion injury.

作　　者：李庆有[1] 路敦跃[1] 张瑞珠[1] 江德华[1] 

机构地区：[1]天津市神经病学研究所神经化学研究室

出　　处：《中风与神经疾病杂志》1997年第3期136-137,共2页Journal of Apoplexy and Nervous Diseases

摘　　要：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。We have investigated batroxobin suppress apoptosis induced by transient cerebral ischemia reperfusion in the rat.The characteristic change of apoptosis DNA strand breaks and morphological changes of apoptotic cells in the hippocampus were detected,using both TdT mediated dUTP biotin nick end labeling(TUNEL) and electron microscopy method,following transient ischemia reperfusion.After 10min of ischemia,the DNA stand breaks and ultrastructural changes of apoptotic cells were present in the hippocampus at 24h of reperfusion and these findings were much more markedly at 48h,96h of reperfusion. After treatment with batroxobin(1.6 Bu/kg,i.v.)the changes mentioned above were significantly reversed.The present study strongly indicate that batroxobin inhibits apoptosis induced by cerebral ischemia reperfusion injury.

关 键 词：巴曲酶 脑缺血再灌流损伤 细胞凋亡 

分 类 号：R743.31[医药卫生—神经病学与精神病学] R973.2[医药卫生—临床医学]