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作 者:王四海[1] 梁春利[1] 张海红[2] 王树[2] WANG Si-hai;LIANG Chun-li;ZHANG Hai-hong;WANG Shu(Department of Cardiothoracic Surgery, the Second Affiliated Hospital of Hebei North University, Xuanhua 075100, China;Department of Pharmacy, Hebei North University)
机构地区:[1]河北北方学院第二附属医院心胸外科,075100 [2]河北北方学院药学系
出 处:《天津医药》2017年第6期593-595,共3页Tianjin Medical Journal
基 金:河北省科技支撑计划项目(07276166);河北北方学院自然科学研究项目(2010022)
摘 要:目的研究大黄酚(Chry)对小鼠脑缺血/再灌注损伤后脑组织内NO的影响及其断头抗缺氧作用。方法将75只SPF级昆明种小鼠随机分为假手术组、模型组、大黄酚高剂量组(Chry 10.0 mg/kg)、中剂量组(Chry 1.0mg/kg)、低剂量组(Chry 0.1 mg/kg)。采用改良Himori法制作小鼠脑缺血/再灌注损伤模型,根据Bederson评分标准测定小鼠神经功能损伤评分。对各组小鼠进行断头抗缺氧实验,记录小鼠喘息时间,并测定脑组织内NO的含量。结果与模型组比较,大黄酚低、中、高剂量组脑缺血再灌注后神经功能损伤评分和脑组织NO含量明显降低,断头抗缺氧的喘息时间(s)明显延长[低剂量组,14.6±1.2;中剂量组,16.4±1.2;高剂量组,17.4±1.1;与模型组(13.2±1.0)比较,均P<0.05]。结论大黄酚可通过减少脑内NO含量和抗缺氧作用对脑缺血/再灌注损伤起到保护效应。Objective To study the effects of chrysophanol(Chry)on NO of brain tissue and anti-anoxia in mice withcerebral ischemia-reperfusion injury.Methods A total of75SPF Kunming mice were randomly allocated into five groups:sham operation group,ischemia-reperfusion group,high-dose group(Chry10.0mg·kg-1),medium-dose group(Chry1.0mg·kg-1)and low-dose group(Chry0.1mg·kg-1).Using improved Himori method,cerebral ischemia reperfusion-injurymodel was produced in conscious mice by temporarily obstructing bilateral common carotid arteries.The neurologicalfunction was measured according to the Bederson scoring standard.The mice were subjected to decapitation for hypoxiatolerance test.The gasping time was measured by anoxia tolerance test in beheaded mice.The level of NO in cerebrum wasdetected.Results Chrysophanol can decrease the level of NO in cerebrum of mice with cerebral ischemia-reperfusioninjury and prolong the gasping time in beheaded mice with cerebral ischemia-reperfusion injury[low-dose group,(14.6±1.2)s;medium-dose group,(16.4±1.2)s;high-dose group,(17.4±1.1)s;ischemia-reperfusion group,(13.2±1.0)s,P<0.05].Conclusion The protective effects of chrysophanol on cerebral ischemia-reperfusion injury are involved in decreasing thecontent of NO in brain tissue and anti-anoxia in mice.
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