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采用给日本大耳白兔大剂量肌注醋酸氢化考的松 8mg·kg-1,造成激素性股骨头缺血坏死的病理模型 ,通过设立骨复生组、模型组、空白组 ,观察血液中红细胞SOD活力及血浆LPO含量的变化 ,发现骨复生具有升高红细胞SOD活力、降低血浆LPO含量的作用。而这些作用是其治疗激素性股骨头缺血坏死的可能机制之一。
A large-dose intramuscular injection of hydrocortisone acetate (8mg·kg-1) was administered to large white rabbits in Japan to cause a pathological model of steroid-induced avascular necrosis of the femoral head. The bone resorption group, model group, and blank group were established to observe red blood cells in the blood. The changes of SOD activity and plasma LPO content found that bone resuscitation has the effect of increasing red blood cell SOD activity and decreasing plasma LPO content. These effects are one of the possible mechanisms for the treatment of steroid-induced avascular necrosis of the femoral head.