摘要
目的:为探讨末端病的发病和修复机制,为寻找有效的防治方法提供实验依据。方法:选取20只Wistar大鼠,末端病组用"电刺激跳跃法"建立动物模型,训练4周后处死,对照组常规喂养。取双后足跟腱,常规HE染色,检测HSP、eNOS和iNOS。结果:末端病组大鼠跟腱部有腱纤维细微裂痕,裂痕周围分别呈红染和蓝染区域,类似玻璃样变性;周围发现大量HSP信号,未见eNOS和iNOS表达,而其它区域可见大量HSP、eNOS和iNOS的表达。讨论:腱纤维局部iN-OS导致的细胞死亡,局部细微裂痕和周围组织细胞变性,可能是造成其损害的主要原因。HSP和eNOS表达促进局部的毛细血管增生,都是促进细胞保护的机制。
Objective：To reveal the injury and repair mechanisms of enthesiopathy,in order to provide evidence for its prevention and treatment.Methods：Twenty Wistar rats were divided into control group（8 rats） and experiment group（12 rats）.After the model of enthesiopathy was established,the rats in model group were trained for 4 weeks before they were sacrificed,while rats in control group were conventionally fed.Achilles tendon of posterior feet in all rats were selected for HE stain and detection of heat shock protein（HSP）,induced nitric oxide synthanse（iNOS） and endothelial nitric oxide synthase（eNOS）.Results：Compared with the control group,there were tendon fiber cracks in Achilles tendon of experiment rats.Around the cracks there was blue and red staining which resembled glassy degeneration.No iNOS or eNOS but HSP expressions were found in those cracks.However,expressions of HSP,iNOS and eNOS were found in other areas.Conclusion：The cell death induced by increase expression of iNOS,the tendon fiber cracks and cell degeneration are possible injury mechanisms in enthesiopathy.The expression of HSP and eNOS are potential mechanism of protection and rehabilitation in enthesiopathy,due to the induced effect of local capillary hyperplasia.
出处
《中国中医骨伤科杂志》
CAS
2010年第4期10-12,共3页
Chinese Journal of Traditional Medical Traumatology & Orthopedics
基金
湖北省自然科学基金项目(2003ABA161)资助
关键词
末端病
损伤
修复
热休克蛋白
一氧化氮合酶
Enthesiopathy
Injury
Repair
Heat shock protein
Nitric oxide synthase
