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目的:观察大鼠脊髓缺血再灌注损伤后应用甲基强的松龙(MP)对脊髓组织钙蛋白酶表达的影响。方法:用纯种雄性成年SD大鼠,夹闭右肾动脉分支下腹主动脉30min后恢复血供,缺血再灌注组(损伤组)不作任何治疗,造成动物脊髓缺血再灌注损伤模型,治疗组于恢复血供后即刻静脉应用MP(治疗组),观察再灌注后3h、24h、72h和7d时脊髓损伤节段钙蛋白酶Ⅰ的表达以及钙蛋白酶特异性底物68-KDNFP的降解。结果:脊髓再灌注后3h出现钙蛋白酶Ⅰ阳性细胞和68-KDNFP的降解产物,随着时间的延长,阳性细胞数目逐渐增多,染色深度逐渐增加,再灌注后72h最明显,MP治疗组较损伤组明显降低(P<0.01)。结论:脊髓再灌注损伤后静脉应用MP可以减少大鼠脊髓中calpain-Ⅰ阳性细胞的表达,对细胞骨架蛋白68-KDNFP具有明显保护作用。证实MP可以抑制钙蛋白酶的表达,可能是MP对脊髓损伤治疗的另一种机理。
Objective: To observe the effect of methylprednisolone (MP) on the expression of calpain in spinal cord after spinal cord ischemia-reperfusion injury in rats. Methods: Pure male adult Sprague-Dawley rats were used to fasten the right atrium of the right renal artery for 30 minutes and then the blood supply was restored. The ischemic reperfusion group (injury group) received no treatment for any reason, resulting in an animal model of spinal cord ischemia-reperfusion injury. Group MP (treatment group) was administered intravenously immediately after blood supply was recovered. The expression of calpain Ⅰ and the degradation of calpain-specific substrate 68-KDNFP at 3h, 24h, 72h and 7d after reperfusion were observed. Results: The expression of calpain Ⅰ positive cells and 68-KDNFP were detected at 3h after reperfusion. The number of positive cells gradually increased and the depth of staining gradually increased after 72h reperfusion. Group was significantly lower (P <0.01). CONCLUSION: MP can decrease the expression of calpain-Ⅰ positive cells in rat spinal cord after spinal cord reperfusion injury and exert obvious protective effect on cytoskeletal protein 68-KDNFP. Confirming that MP can inhibit the expression of calpain may be another mechanism by which MP can treat spinal cord injury.