双苯氟嗪对大鼠全脑缺血再灌注损伤的保护作用

目的研究双苯氟嗪(D ip)对大鼠急性全脑缺血再灌注损伤的保护作用,并初步探讨其作用机制。方法采用Pu lsinelli等的四动脉结扎法(4-VO)造成大鼠全脑缺血再灌注损伤模型,观察大鼠全脑缺血再灌注损伤后早期脑组织水分的变化、生化指标的改变,再灌注后期行为学和组织形态学的改变。结果缺血30 m in再灌注1 h脑组织水分及丙二醛(MDA)含量升高,乳酸脱氢酶(LDH)和超氧化物歧化酶(SOD)活性下降;缺血20 m in再灌注5 d后海马CA1区椎体细胞层破裂,胞核固缩或溶解,间质也变得疏松。行为学实验表明大鼠记忆力明显受损。D ip可不同程度地抑制上述变化,能对抗自由基损伤和脑水肿,并能保护海马CA1区神经元免受缺血损伤,提高大鼠对空间辨别的记忆能力。结论D ip对大鼠全脑缺血再灌注早期损伤有明显的保护作用,并能保护海马CA1区神经元免受缺血损伤,提高大鼠对空间辨别的记忆能力,对迟发性神经元死亡有一定的保护作用。这可能与其抗脂质过氧化产物产生有关。

Protective effects of dipfluzine against the whole cerebral ischemia and reperfusion injury in rats

Aim To study the protective effects of dipfluzine against the whole cerebral ischemia and reperfusion injury and its mechanisms. Methods Four-vessel occlusion method was used to make the cerebral ischemia-reperfusion model. In early period of reperfusion, several including LDH, MDA, SOD and brain water content were tested. And in the late period of reperfusion, the delayed neuronal death and amnesia induced by reperfusion were studied. Results The contents of brain water and MDA were increased, and the activities of SOD and LDH were decreased after ischemia and reperfusion injury. The hippocampal structureand memory of rats were also destroyed in the delayed neuronal death. Dip reversed the changes obviously. It had antagonistic effect on brain edema and lipid oxidation,it also protected the neurons of hippocampal CAI regions from ischemia injury. Conclusion Dip had protective effects on the early stage of reperfusion injury, and delayed neuronal death after the whole cerebral ischemia and reperfusion the antagonistic effect on , which were possibly due to lipid peroxidation.