摘要
目的研究iNOS在压疮大鼠骨骼肌中表达情况,探讨iNOS参与压疮发生的机制。方法54只Wistar大鼠随机分为9组:对照组、缺血再灌注组(IR组):IROh组、IR4h组、IR12h组、IR24h组、IR3d组、IR1周组、IR2周组、IR4周组,每组6只。免疫组化法观察大鼠骨骼肌iNOS阳性纤维数量及形态学变化;免疫印迹法检测骨骼肌iNOS蛋白表达情况。结果实验组大鼠骨骼肌的结构发生进行性损伤,出现肌纤维溶解、断裂、空泡变、水肿、横纹消失、血管扩张充血、间质水肿等病理改变。以IR24h最为严重,此后逐渐缓解,至IR4周组织损伤仍未完全修复。在IR4h组、IR12h组、IR24h组、IR3d组中可见大量iNOS阳性表达的骨骼肌纤维,和对照组相比iNOS蛋白表达水平显著增高(P〈0.05)。IRl2h组、IR24h组iNOS表达水平最高。结论iNOS参与压疮的形成,其活化是压疮缺血再灌注损伤过程中自由基氧化损伤的重要环节。
Objective To investigate the expression of inducible nitric oxide synthase(iNOS) in skeletal muscle of rats with pressure ulcer,and to explore its roles in the development of pressure ulcer.Methods 54 Wistar rats were randomly divided into 9 groups: nonischemia control group and ischemia-reperfusion groups(IR group} IR0h group, IR4h group, lR12h group, IR24h group, IR3d group, IR1w group, IR2w group, IR4w group,every group had six rats.iNOS protein expression in local muscle was examined by immunohistochemistry, iNOS protein expression was examined by immunoblotting.Results There was progressive impairment of skeletal muscle, such as dissolve, rupture, edema, disappeared transverse striation, hemangiectasis and congestion, interstitial edema.The skeletal muscle injury reached the peak at IR24h,then relieved gradually,but couldn't recover till IR4w.There was iNOS expression in skeletal muscle of IR4h group, IRl2h group, IR24h group, IR3d group,the expression in the four groups was higher than which in control group(P〈0.05).The level of iNOS in skeletal muscle reached the peak at 12h and 24h.Conclusions iNOS participates in the process of pressure ulcer, the activation of iNOS is the important segment of flee radical injury in ischemia reperfusion injury of pressure ulcer.
出处
《中国血液流变学杂志》
CAS
2009年第3期362-365,F0002,共5页
Chinese Journal of Hemorheology
关键词
压疮
诱导型一氰化氮合酶
一氧化氮
骨骼肌
pressure ulcer
inducible nitric oxide synthase
nitric oxide
skeletal muscle