摘要
目的:观察辛伐他汀对局部脑缺血损伤大鼠的神经保护作用及其线粒体机制。方法:实验于2005-03/08在广州医学院生理实验室进行。取72只SD雄性大鼠,随机分为正常对照组、缺血模型组、辛伐他汀组3组,每组24只。辛伐他汀组大鼠灌胃辛伐他汀20mg/kg,1次/d,连续7d,最后一次灌胃1h后缺血模型组和辛伐他汀组大鼠线栓法复制左侧脑缺血2h再灌注模型,正常对照组仅分离动脉,不缺血。观察各组大鼠术后24h神经功能评分(3～18分,评分越高越好)、脑含水量、脑梗死体积以及脑组织线粒体超氧化物歧化酶、丙二醛、NO和Na+-K+ATPase的改变。结果:经补充后72只大鼠进入结果分析。①神经功能评分:辛伐他汀组明显高于缺血模型组(15.87±0.83,14.25±0.71,P<0.01)。②脑含水量:辛伐他汀组明显低于缺血模型组[(79.56±1.14)%,(81.13±1.36)%,P<0.05]。③脑梗死体积:辛伐他汀组明显低于缺血模型组[(173.7±15.92),(239.94±22.01)mm3,P<0.01]。④脑组织线粒体超氧化物歧化酶和Na+-K+ATPase活性:辛伐他汀组明显高于缺血模型组(P<0.05)。⑤脑组织线粒体丙二醛和NO含量:辛伐他汀组明显低于缺血模型组(P<0.01)。结论:辛伐他汀可能通过抑制大脑中动脉阻断后引起的脑内线粒体脂质过氧化反应,减少自由基的生成,稳定线粒体功能,增加ATP的生成,从而对缺血脑组织产生保护作用。
AIM： To observe the neuroproteetive effect of simvastatin against focal cerebral ischemic injury in rats and its mitochondrial mechanisms. METHODS： The experiment was conducted in the physiological laboratory of Guangzhou Medical College from March to August 2005. Seventy-two male SD rats were randomly divided into normal control group （n=24）, ischemic model group （n=24） and simvastatin group （n=24）. Rats in the simvastatingroupweretreatedwithgastricperfusionofsimvastatin 120 mg/kg）, once a day for 7 continuous days. Models of left cerebral ischemia （2 hours）-reperfusion were duplicated at 1 hours after the last gastric perfusion in the ischemic model group and simvastatin group, and the rats in the normal control group were only treated by arterial isolation but no ischemia. The neurologic function score （3-18 points, the higher the better）, brain water content, infarction volume and the changes of the activity of superoxide dismutase （SOD） and concentrations of malondialdehyde （MDA） and nitric oxide, activity of Na^＋-K^＋ ATPase in the mitochondria of brain tissue were observed at 24 hours postoperatively in all the groups. RESULTS： Finally, 72 rats were involved in the analysis of results after complement. ①Neurological score： It was obviously higher in the simvastatin group than in the ischemic model group （15.87±0.83, 14.25 ±0.71, P 〈 0.01）.② Brain water content： It was obviously lower in the simvastatin group than in the ischemic model group [（79.56±1.14）%, （81.13±1.36）%, P 〈 0.05]. ③ Infarction volume： It was obviously lower in the simvastatin group than in the isehemic model group [（173.7 ±15.92）, （239.94±22.01） mm^3, P 〈 0.01]. ④Activities of SOD and Na^＋- ATPase in the mitochondria of brain tissue： Those were obviously higher in the simvastatin group than in the ischemic model group （P 〈 0.05）. ⑤ Concentrations of MDA and nitric oxide in the mitochondria of brain tissue： Those were obviously lower in the s
出处
《中国临床康复》
CSCD
北大核心
2006年第6期82-84,i0002,共4页
Chinese Journal of Clinical Rehabilitation
