氧化应激对激素性股骨头缺血坏死微血管的损伤作用

Microvascular injury of femoral head avascular necrosis caused by steroid-induced oxidative stress

目的探讨氧化应激在激素性股骨头缺血坏死微血管损伤中的作用。方法选择不同原因的股骨头缺血坏死患者30例,按病因分为A组(激素性)、B组(酒精性)和C组(特发性),每组10例;另选10例股骨颈骨折患者设为D组(正常对照)。测定血清总抗氧化能力(T-AOC)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)、还原型谷胱甘肽(GSH)、丙二醛(MDA),观察氧化应激水平;Verhoeff氏染色法观察微血管损伤情况;透射电镜观察股骨头组织的超微结构。结果A组T-AOC、SOD、GSH-PX、GSH、MDA水平较其他组变化显著(P<0.05),其他组间无显著差异;Verhoeff氏染色结果显示A组微动脉损伤阳性率明显高于其他组(P<0.05),其他组间无显著差异;透射电镜下A组骨组织中微动脉管壁不完整,闭锁的微动脉多见,内皮细胞结构不清,凋亡细胞多见,较B、C组损伤程度重。结论氧化应激可能通过微动脉损伤途径在激素性股骨头缺血坏死的发病中起重要作用。

Objective To explore the microvascular injury of femoral head avascular necrosis caused by steroid-induced oxidative stress. Methods Thirty patients with multiple-cause avascular necrosis of femoral head were selected and divided into 3 groups （10 in each group） ： Group A （hormone group）, Group B （alcoholic group） and Group C （idiopathic group）. Group D served as control group. We determined serum total-antioxidative capability （T-AOC）, superoxide dismutase （SOD）, glutathione peroxidase （GSH-PX）, glutathione （GSH） and malondialdehyde （MDA） to observe the level of oxidative stress. Microvascular injury was observed by Verhoeff staining. Transmission electron microscope was used to observe the ultrastructure of the femoral head. Results In Group A, T-AOC, SOD, GSH-PX, GSH and MDA levels changed more obviously than those in the other groups （P〈0. 05）, and there were no significant differences among the other groups. Verhoeff staining showed that the positive rate of arteriole damage in Group A was significantly higher than that in the other groups （P〈0. 05）, and there were no significant differences among the other groups. Under the transmission electron microscope, bone tissue arteriole wall in Group A was not complete, with more atresic arterioles, unclear endothelial cell structure and more apoptotic cells than in Groups B and C. Conclusion Oxidative stress may damage the artery through microchannels in steroid-induced avascular necrosis and plays an important role in the pathogenesis.