摘要目的 探讨二氮嗪对幼龄大鼠深低温脑缺血再灌注后氧自由基和细胞凋亡的影响及相关的脑保护作用机制.方法 将54只3周龄健康sD大鼠随机分为假手术组、模型组和二氮嗪组,每组18只,建立深低温脑缺血再灌注模型.于术后24 h处死大鼠,检测脑组织超氧化物歧化酶(SOD)、丙二醛的含量,Western Blot法检测脑组织细胞质细胞色素C含量,免疫组化法检测脑组织细胞质Caspase-3含量.结果 模型组脑组织中SOD含量为(198±41)U/mg,低于假手术组的(321±36)U/rag(P<0.01);丙二醛含量为(212±21)nmol/mg,高于假手术组的(100±23)nmol/mg(P<0.01);细胞色素C蛋白表达(0.72±0.09)和Caspase-3蛋白表达(83±10)均高于假手术组(0.17±0.02和115±9)(P<0.01).二氮嗪组脑组织SOD含量为(264±34)U/rag,高于模型组(P<0.05);而丙二醛含量(174±19)nmol/mg、细胞色素C蛋白表达(0.41±0.05)和Caspase-3蛋白表达(99±11)均低于模型组(P<0.05).结论 二氮嗪对幼龄大鼠深低温脑缺血再灌注损伤具有脑保护作用,其机制与抑制氧自由基产生和细胞凋亡有关.

abstractsObjective To determine the effects of diazoxide on oxygen free radicals and cell apoptosis in brain tissue after deep hypothermia cerebral ischemia reperfusion injury in young rats. Methods Fifty-four 3-week-old Sprague-Dawley rats were randomly and equitably divided into sham-operated group,model group and diazoxide group respectively ( n = 18 ). The model of hypothermia cerebral ischemia reperfusion injury was made. After 24 hours of operation, the brains of rats were removed and preserved.The content of superoxide dismutase (SOD) and malonaldehyde (MDA) in brain tissue were detected.Cytosolic C release of cytochrome was confirmed by Western Blot. The protein expression of Caspase-3 was determined by immunohistochemistry. Results In the model group, the content of SOD was ( 198 ± 41 )U/rag, lower than the sham-operated group' s (321 ± 36) U/mg ( P < 0. O1 ). The content of MDA was (212±21 ) nmol/mg, was higher than the sham-operated group's (100±23) nmol/mg (P <0. O1 ), andthe expressions of cytochrome C (0. 72 ±0. 09) and Caspase-3 (83 ± 10) were all significantly higher than those in the sham-operated group (0. 17 sO. 02 and 1 15 ± 9) (P < O. 01 ). Compared with the model group,the content of SOD in the diazoxide group [ (264±34) U/rag ] was markedly increased ( P < 0. 05 ). In addition, diazoxide provided significant reductions in the content of MI)A [ ( 174 ± 19) nmol/mg] and theexpressions of cytochrome C ( 0. 41 ± 0. 05 ) and Caspase-3 ( 99 ± 11 ) ( P < 0. 05 ). Conclusions The neurooprotective effects of diazoxide against brain injury induced by deep hypothermia cerebral ischemia reperfusion through inhibiting oxygen free radicals and cell apoptosis. Diazoxide may become a new neuroprotective drug after infant complicated congenital cardiac operation.