缺血-再灌注对甲床损伤机制实验研究.docVIP

缺血-再灌注对甲床损伤机制实验研究 　　[摘要] 目的 探讨使用止血带后缺血-再灌注对甲床组织的损伤及其相应的作用机制。 方法 大耳白兔于右后肢根部上止血带，于缺血30、60、90、120 min再灌注1 h后剥离甲床组织。分光分析法检测标本中超氧化物歧化酶（SOD）活性。荧光定量PCR检测标本中TNF-α基因的mRNA表达水平。TUNEL法检测细胞凋亡。 结果 甲床组织缺血30 min后再灌注SOD活力、TNF-α mRNA表达和细胞凋亡率无显著改变（P 0.05）。与缺血30 min比较，缺血60 min后再灌注甲床组织SOD活力显著降低（P 0.05）。 结论 缺血60 min后再灌注可以诱发甲床细胞凋亡的发生，可能是术后指甲畸形的主要致病机制，SOD的减少和TNF-α表达的升高是导致细胞凋亡的主要原因。 　　[关键词] 甲床损伤；缺血再灌；指甲畸形 　　[中图分类号] R758.72 [文献标识码] A [文章编号] 1673-7210（2012）02（c）-0029-02 　　 　　Study of ischemia-reperfusion injury on nail bed and its mechanisms 　　OU Chunpei LI Chunye LI Xiaowen CHEN Guoyi JIA Saixiong 　　Department of Upper Limbs Micro-Surgery, Shenzhen Bao′an Hospital Affiliated to South Madical University, Guangdong Province, Shenzhen 518101, China 　　[Abstract] Objective To investigate the effects of ischemia-reperfusion injury on nail bed by tourniquet and its mechanisms. Methods The model of nail bed ischemia-reperfusion injury was established by using rabbit which were used tourniquet on the right back leg. The activity of SOD was detected by spectrophotometer. Real-time PCR was used to detect the mRNA expression of TNF-α. The apoptosis was detected by TUNEL analysis. Results The the SOD activity, TNF-α mPNA expression, and apoptosis were not change by ischemia 30 min and reperfusion in nail bed tissue. Compared with 30 min, the SOD activity was decreased by ischemia 60 min and reperfusion in nail bed tissue (P 0.05). Conclusion The ischemia 60 min and reperfusion injury is a important reason to induce apoptosis in nail bed tissue, may be the main mechanism of nail duplication after operation. The low SOD activity and high TNF-α mRNA expression are the main reasons to induce apoptosis. 　　[Key words] Nail bed injury; Ischemia-reperfusion; Nail duplication 　　 　　缺血-再灌注（ischemia-reperfusion，I/R）所致人体各个组织和器官的损伤在临床并不少见，包括术中为避免出血??为阻断组织和器官的供血后再灌注的损伤。如骨科常用止血带限时地压迫主要供血血管而达到四肢手术和创伤出血中的止血，临床中笔者观察到手外伤患肢正常使用止血带，缺血再灌注后未受伤手指指甲也会出现畸形生长，其机制尚不清楚。本研究在动物模拟实验的基础上探讨使用止血带后缺血再灌注对甲床的损伤及其相应的作用机制。 　　1 材