摘要
目的:观察硫酸镁(MgSO4)对小鼠全脑缺血再灌注损伤后一氧化氮(NO)和ATP酶的影响,探讨其保护作用及机制。方法:昆明小鼠100只,随机分成假手术组、缺血再灌注模型组和MgSO4低剂量组、中剂量组、高剂量组。采用结扎双侧颈总动脉及加压颈部软组织的方法复制全脑缺血再灌注模型,缺血30 min再灌注1 h。观察各组小鼠脑组织NO含量、一氧化氮合酶(NOS)和诱导型一氧化氮合酶(iNOS)活性,Ca2+-Mg2+-ATP酶和Na+-K+-ATP酶活性及病理学变化。结果:MgSO4各组脑组织NO含量和NOS、iNOS活性明显低于缺血再灌注模型组,高于假手术组(P<0.05~P<0.01),并能提高Ca2+-Mg2+-ATP酶和Na+-K+-ATP酶活性(P<0.05~P<0.01)。结论:MgSO4预处理能显著降低小鼠脑缺血再灌注后NO含量和NOS活性,并提高Ca2+-Mg2+-ATP酶和Na+-K+-ATP酶活性,从而减轻脑缺血再灌注损伤。
Objective:To explore the protective effect and mechanism of magnesium sulfate on global cerebral ischemia/reperfusion injury on mice.Methods:One hundred KM mice were randomly divided into sham operation group,ischemia/reperfusion group and magnesium sulfate groups(low dosage group,medium dosage group and high dosage group).Global cerebral ischemia was made by blocking bilateral common carotid artery and pressing soft tissues in carotid for 30 min.After one-hour reperfusion,the mice were killed.The content of nitric oxide(NO),activities of nitric oxide synthase(NOS),Ca2+-Mg2+-ATPase and Na+-K+-ATPase were measured and the pathologic changes of the brain tissues were observed.Results:Compared to ischemia/reperfusion group,NO content and NOS activity of brain tissue decreased the different dosages of magnesium sulfate,and enhance the activities of Ca2+-Mg2+-ATPase and Na+-K+-ATPase(P0.05-P0.01).Conclusions:The pretreatment of magnesium sulfate could obviously relieve cerebral ischemia/reperfusion injury by decreasing the content of NO and activity of NOS and increasing the activities of Ca2+-Mg2+-ATPase and Na+-K+-ATPase.
出处
《蚌埠医学院学报》
CAS
2010年第4期330-333,共4页
Journal of Bengbu Medical College
基金
安徽省教育厅自然科学研究资助项目(KJ2008B105ZC)