论文部分内容阅读
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.