血晶素促进缺血缺氧大鼠脑组织诱导型血红素氧合酶基因的表达

目的研究血晶素对全脑缺血再灌注Wistar大鼠脑保护作用及机制.方法成功建立成年Wistar大鼠全脑缺血再灌注模型后,于全脑缺血10 min再灌注24、48、72 h 3个时相点观察缺血再灌注对大鼠脑组织血红素加氧酶-1(heme oxygenase-1,HO-1)蛋白表达及皮质神经元的作用及变化规律;并于模型成功建立后5 min,1、2 d侧脑室内注射25mg/kg的血晶素,观察血晶素对缺血再灌注大鼠脑HO-1蛋白表达及皮质神经元的影响.结果大鼠脑组织HO-1蛋白表达在全脑缺血10 min再灌注48 h达高峰(P＜0.05);血晶素可促进脑HO-1蛋白表达(P＜0.05),并减轻了全脑缺血再灌注所导致的皮质损害.结论血晶素对缺血再灌注大鼠脑缺血有保护作用,其可能的机制是通过上调脑HO-1蛋白表达,启动一系列的内源性的神经保护机制来发挥脑保护作用.

Neuroprotective effect of heme oxygenase-1 induced by hemin in the brain of rats suffered from ischemia-reperfusion injury

Objective To investigate the neuroprotective effect of heme oxygenase-1 induced by hemin on the rat brain after ischemia-reperfusion. Methods The global cerebral ischemia-reperfusion model in 48 Wistar rats was surgically prepared by four-vessel occlusion method (4-VO) and another 8 rats underwent sham-operation as normal control. Hemin was injected over 5 min at the lateral ventricle at 15 min, 24 h and 48 h after reperfusion in 24 ischemia-reperfusion rat models and normal saline was applied to another 24 rat models at the same time points as negative control. The effect of hemin was evaluated on the pathologic outcome and on the immuohistochemical reaction for HO-1 after 10-minute global cerebral ischemia followed by 24 h, 48 h and 72 h reperfusion. Results The peak level of HO-1-like immunoreactivity was found at 48 h after the reperfusion as compared with the matched rats in normal saline group (P<0.05). Hemin significantly increased viable neurons in the cortex and striatum as compared to that of normal saline group (P<0.05). Conclusion The induction of HO-1 protein by the administration of hemin may contribute to cellular defense against ischemic damage in brain regions where potential ability to synthesize HO-1 is retained in ischemia.