大蒜新素对脑缺血再灌注大鼠海马的保护作用

目的探讨大蒜新素对脑缺血再灌注海马组织的保护作用与钙转运的关系。方法采用4血管闭塞法制备大鼠全脑缺血再灌注模型,大蒜新素10,20和30mg.kg-1分2次于缺血前30min和再灌注后10min经尾静脉注入,每次注射总量的1/2。再灌注后24h取大鼠海马,甲苯胺蓝染色显微镜下观察海马组织学改变及存活神经元密度;定磷比色法测定Ca2+-转运ATP酶活性;原子吸收法测定钙含量。结果全脑缺血10min再灌注24h时,海马CA1区形态学改变明显,神经元密度明显降低;海马组织Ca2+-转运ATP酶活性降低;组织钙含量显著增加。静脉给予大蒜新素可使缺血再灌注海马组织形态学改变程度明显减轻,存活神经元密度增加,Ca2+-转运ATP酶活性增加,组织钙含量降低。结论大蒜新素对全脑缺血再灌注后海马组织具有明显的保护作用;增加Ca2+-转运ATP酶活性、减少组织钙含量可能是其保护作用的机制之一。

Protective effect of allitridi against cerebral ischemia- reperfusion injury in rat hippocampus

AIM To explore the relation of the protective effect of allitridi against cerebral ischemia-reperfusion injury and the Ca²⁺ transporting mechanism in hippocampal neurons of rats. METHODS The global cerebral ischemia-reperfusion models were established by 4-vessel occlusion. Allitridi 10, 20 and 30 mg·kg^-1 was injected through rat tail vein, half dose at 30 min before brain ischemia and another half dose at 10 min after reperfusion, respectively. The hippocampus of rat was removed 24 h after reperfusion. Toluidine blue staining was used to investigate histological grade and survival neuronal density of hippocampal CA1 subfield by microscope. The Pi-colorimetric method was used to measure the activity of Ca²⁺ -transporting ATPase. Atomic absorption was used for analysis of Ca²⁺ content in hippocampal tissue. RESULTS Ten minutes cerebral ischemia then reperfusion for 24 h resulted in distinguished morphological changes and the decrease in survival neuronal density of hippocampal CA1, and induced the depression in Ca²⁺ - transporting ATP enzyme activity and increase in Ca²⁺ content of hippocampal tissue. Allitridi intravenous administration significantly lightened the damage in hippocampal tissue induced by cerebral ischemia-reperfusion and increased the survival neuronal density. At the same time, allitridi remarkably increased the Ca²⁺ -transporting ATPase activity and reduced Ca²⁺ content of hippocampal tissues of ischemic-reperfused rats. CONCLUSION Reducing Ca²⁺ content in hippocampal neuron by increasing the activity of Ca²⁺ -transporting ATPase maybe one of the protective mechanisms of allitridi against cerebral ischemia-reperfusion injury.