CAJ | 학술논문

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4 h后,再灌注1,2,4,8,12 h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.
배경:골격기결혈재관주손상적치료방법일직시골과의생문연구적중점화난점.목적:관찰초양화물기화매모형배합물(MSODa)대골격기결혈재관주(I/R)후적보호작용,병대기보호궤제진행탐토,위골격기적손상수복제공이론의거.설계:수궤대조실험.지점화재료:재합이빈의과대학부속제이의원완성.청길급웅성Wistar대서96지,체질량(200±20)g,유합이빈의과대학부속제이의원동물실험중심제공.간예:건립대서후지결혈재관주모형,장96지대서수궤분위정상대조조(n=6)、결혈재관주조(n=30)、생리염수조(n=30)、MSODa조(n=30).결혈재관주조,생리염수조,MSODa조분별재결혈4 h후,재관주1,2,4,8,12 h말,측정각항지표.주요관찰지표:측정혈장중적병이철、골격기조직중적수과양화물매(MPO),백세포상β2정합소(CD11b/CD18)화골격기혈관중세포간점부분자(ICAM)-1적표체정황급각조적조직학개변.결과:Ⅱ조각시상점MDA,MPO,CD11b/CD18,ICAM-1적표체균교Ⅰ조유비상현저승고,골격기조직손상야수재관주시간적연장이축점가중,Ⅳ조칙가이명현억제저충변화.결론:MSODa통과감소자유기적생성,억제점부분자적표체이감경골격기I/R손상.
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 studySETTING 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(group Ⅰ, n = 6), ischemia-repeffusion group (group Ⅱ, 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 group Ⅱ, groupⅢ, and groupⅣ.MAIN OUTCOME MEASURES: Malondialdehyde(MDA) in plasma,myeloperoxidase(MPO) in skeletal muscle, CD11b/CD18 on leukocytes,and intercellular adhesion molecule-l(ICAM-1) in skeletal muscular yessels, 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 group Ⅱ compared with group Ⅰ. 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-repeffusion injury by inhibiting the production of free radicals and the expression of adhesion molecules.