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作 者:杨克[1] 李龙[1] 乔中原[1] 樊荣[1] 杨林[2]
机构地区:[1]西安市第一医院麻醉科,陕西西安710002 [2]资阳市第一人民医院放射科,四川资阳641300
出 处:《现代生物医学进展》2017年第17期3246-3249,共4页Progress in Modern Biomedicine
基 金:国家自然科学基金青年基金项目(81401138)
摘 要:目的:研究orexin-A对缺血再灌注大鼠脑损伤的保护作用。方法:取成年雄性大鼠6只,观察MCAO前和MCAO后2 h、24h的生理学参数,界定后续指标参考时间。另取20只大鼠随机分为MCAO组、vehicle组、orexin-A 50μg/kg组和orexin-A 100μg/kg组(n=5),于缺血再灌注24 h后评估大鼠神经功能学评分和脑梗死容积。再取60只大鼠同样分成4组,(各组n=15),每组在术前、手术后6 h、24 h(各时间点n=5)取脑组织匀浆离心,检测上清液中谷胱甘肽过氧化物酶(GSH-PX)和丙二醛(MDA)的含量。结果:(1)大鼠MCAO术前、术后2 h、24 h生理参数比较无统计学意义(P>0.05),提示脑保护参考指标在MCAO后24 h内不受影响。(2)与MCAO组、vehicle组相比,orexin-A 50和100μg/kg降低神经功能评分(P<0.05)且梗死容积缩小(P<0.05);术前、术后6 h和术后24 h,脑匀浆中GSH-PX活性升高,MDA含量降低(P<0.05)。结论:Orexin-A可能通过降低脑内自由基水平,控制脂质过氧化物酶从而对脑缺血再灌注损伤起保护作用。Objective: To evaluate the protective effect of orexin-A on the cerebral ischemia reperfusion injury in rats. Methods: The physiological parameters were observed to define time rang by six rats before MCAO and after MCAO 2 h, 24 h. Twenty rats were randomly divided into middle cerebral artery occlusion (MCAO) group, vehicle group, orexin-A 50 μg/kg and orexin-A 100 μg/kg group (n=5). Neurological dysfunction scores (NDS) and infarct volume were measured at 24h after ischemia-reperfusion. The other sixty rats were also divided into 4 groups (n=15 each group), the level of glutathione peroxidase (GSH-PX) and maleic diadehyde (MDA) in brain plasm were detected pre-operation and at 6 h, 24 h after ischemia-reperfusion (n=5 each time point). Results: ONo significant differentce was found in the pyhsiological parameters of rats before MCAO and at 2 h, 24 h after MCAO (P〉0.05), suggesting that the follow indexes of cerebral protection hadn't been influenced within 24 h after MCAO. ②Compared with the MCAO group and vehicle group, the NDS (P〈0.05) and the percentage of brain infarct were better in the orexin-A 50 and 100 μg/kg group (P〈0.05); the concentration of GSH-PX was increased and MDA was decreased in orexin-A 50 and 100 μg/kg group (P〈0.05). Conclusion: Orexin-A might play a protective role in the cerebral ischemia reperfusion injury in rats by increasing the concentration of antiperoxidase and decreasing the level of oxygen flee radicals.
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