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研究巴曲酶对脑缺血再灌注所致延迟性神经元死亡的影响以及与OH·产生的关系. 沙土鼠前脑缺血10 m in 再灌注60 m in. 应用高效液相色谱法测定纹状体多巴胺,海马ATP和2,3-二羟基苯甲酸(2,3-DHBA, 反映OH·含量)的含量. 应用病理方法检查海马CA1 区锥体细胞延迟性死亡情况.结果显示, 在再灌注开始时ip 巴曲酶8 BU·kg- 1明显促进海马ATP含量的恢复,减少OH·的产生和纹状体多巴胺的释放. 脑缺血再灌注后d 7 巴曲酶组(8 BU·kg- 1 ip,每日1 次,共3 d)海马CA1 区存活的锥体细胞数目也明显多于对照组(每100 平方微米0.27±0.11 vs 0.04±0.03). 以上结果提示, 巴曲酶可减轻脑缺血再灌注所致的延迟性神经元死亡, 其机理可能与其减少脑缺血再灌注期间OH·的产生有关.
To study the effect of batroxobin on delayed neuronal death induced by cerebral ischemia-reperfusion and its relationship with OH · production. Gerbils forebrain ischemia 10 m in reperfusion 60 m in. The levels of striatum dopamine, hippocampal ATP and 2,3-dihydroxybenzoic acid (2,3-DHBA, OH · content) were determined by high performance liquid chromatography. Pathological examination of pyramidal cells in hippocampal CA1 area delayed death. The results showed that at the beginning of reperfusion, ip-batroxobin 8 BU · kg-1 significantly promoted the recovery of ATP content in hippocampus and reduced the production of OH · and the release of striatum dopamine. The number of pyramidal neurons surviving in the CA1 hippocampus was also significantly increased in the d 7 batroxobin group (8 BU · kg-1 ip, once daily for 3 days) after cerebral ischemia / reperfusion 0.27 ± 0.11 vs 0.04 ± 0.03). The above results suggest that batroxobin can reduce the delayed neuronal death caused by cerebral ischemia and reperfusion, and its mechanism may be related to its reduction of OH · during cerebral ischemia and reperfusion.