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作 者:王新涛[1] 吕松岑[1] 韩竹[1] 关德宏[1] 常曼丽[1]
机构地区:[1]哈尔滨医科大学附属第二医院骨外科,黑龙江省哈尔滨市150086
出 处:《中国临床康复》2004年第29期6542-6544,共3页Chinese Journal of Clinical Rehabilitation
基 金:黑龙江省自然基金资助(D9827)~~
摘 要:背景:骨骼肌缺血再灌注损伤的治疗方法一直是骨科医生们研究的重点和难点。目的:观察超氧化物歧化酶模型配合物(MSODa)对骨骼肌缺血再灌注(I/R)后的保护作用,并对其保护机制进行探讨,为骨骼肌的损伤修复提供理论依据。设计:随机对照实验。地点和材料:在哈尔滨医科大学附属第二医院完成。清洁级雄性Wistar大鼠96只,体质量(200±20)g,由哈尔滨医科大学附属第二医院动物实验中心提供。干预:建立大鼠后肢缺血再灌注模型,将96只大鼠随机分为正常对照组(n=6)、缺血再灌注组(n=30)、生理盐水组(n=30)、MSODa组(n=30)。缺血再灌注组,生理盐水组,MSODa组分别在缺血4h后,再灌注1,2,4,8,12h末,测定各项指标。主要观察指标:测定血浆中的丙二醛、骨骼肌组织中的髓过氧化物酶(MPO),白细胞上β2整合素(CD11b/CD18)和骨骼肌血管中细胞间黏附分子(ICAM)-1的表达情况及各组的组织学改变。结果:Ⅱ组各时相点MDA,MPO,CD11b/CD18,ICAM-1的表达均较Ⅰ组有非常显著升高,骨骼肌组织损伤也随再灌注时间的延长而逐渐加重,Ⅳ组则可以明显抑制这种变化。结论:MSODa通过减少自由基的生成,抑制黏附分子的表达而减轻骨骼肌I/R损伤。BACKGROUND:Treatment of skeletal muscle ischemia reperfusion injury has been an important and difficult task for orthopedicians. OBJECTIVE:To explore the protective function and mechanism of superoxide dismutase(SOD) model coordination compounds MSODa in skeletal muscle ischemia reperfusion injury,and thus provides a theoretical basis for the rehabilitation of skeletal muscle injury. DESIGN:Randomized controlled study SETTING and MATERIALS:The experiment was completed in the Second Hospital affiliated to Harbin Medical University.Ninety six clean Wistar rats,with the mean mass of(200±20) g,were provided by the experimental animal center of the Second Hospital affiliated to Harbin Medical University. INTERVENTIONS:Rat hind limb ischemia reperfusional models were successfully established.Ninety six rats were randomly divided into four groups: normal control group(groupⅠ,n=6),ischemia reperfusion group (groupⅡ, n=30),normal saline group (groupⅢ,n=30),and MSODa group(group Ⅳ,n=30).The pathological changes were assessed 4 hours after ischemia, and 1 hour,2 hours,4 hours,8 hours,and 12 hours after reperfusion in groupⅡ,groupⅢ,and groupⅣ. MAIN OUTCOME MEASURES:Malondialdehyde(MDA)in plasma, myeloperoxidase(MPO) in skeletal muscle,CD11b/CD18 on leukocytes, and intercellular adhesion molecule 1(ICAM 1) in skeletal muscular vessels,as well as the pathological changes of each group were measured. RESULTS:The expression of MDA,MPO,CD11b/CD18,and ICAM 1 increased significantly in groupⅡ compared with groupⅠ.Skeletal muscle injury aggravated along with the extension of reperfusion time,but such changes were significantly improved in group Ⅳ. CONCLUSION:MSODa can prevent skeletal muscle ischemia reperfusion injury by inhibiting the production of free radicals and the expression of adhesion molecules.
关 键 词:骨骼肌缺血 大鼠 血再灌注损伤 MSOD 保护作用 表达 MPO 酶模型 清洁级 雄性
分 类 号:R743[医药卫生—神经病学与精神病学] R285.5[医药卫生—临床医学]
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