甲基强的松龙对脊髓损伤后伤段脊髓线粒体功能的影响

Effects of methylprednisolone on mitchondrial function of injured spinal cord

目的：探讨脊髓损伤后伤段脊髓线粒体呼吸功能和线粒体内游离钙的变化和早期使用甲基强的松龙(MP)对其的影响。方法：54只SD大鼠，随机分组为假手术组(对照组)、脊髓损伤组(SCI组，采用Allen’s打击法造成大鼠脊髓损伤模型)和脊髓损伤后应用MP治疗组(MP组)，每组又分为处理后6h、12h、24h三个时间相，每个时间相6只。在各时间相处死动物后提取伤段脊髓线粒体，测定线粒体呼吸Ⅲ态(R3)、呼吸Ⅳ态(R4)、呼吸控制率(RCR)、磷氧比(P／O)和线粒体内游离Ca^(2+)浓度。结果：SCI组在伤后6h、12h和24h R3、RCR和P／O显著低于对照组，R4和线粒体内游离Ca^(2+)浓度显著高于对照组，差异有显著性(P＜0．01)；伤后6h和12h MP组R3、RCR和P／O高于SCI组，R4和线粒体内游离Ca^(2+)浓度低于SCI组，差异有显著性(P＜0．01)；MP组R3、R4和RCR在6h和12h时与对照组之间无显著性差异，24h时R3、RCR和P／O低于正常对照组，有显著性差异(P＜0．05)。结论：脊髓损伤后伤段脊髓线粒体呼吸功能和线粒体内游离Ca^(2+)浓度明显受到影响，线粒体内膜通透性增加，线粒体氧化磷酸化的偶联程度明显受到抑制。早期使用甲基强的松龙可明显改善线粒体的呼吸功能。抑制Ca^(2+)内流，保护伤段脊髓线粒体的稳定性。

Objective：To study the effects of methylprednisolone on the injured spinal cord mitchondrial function in experimental spinal cord injury（SCI） model and its possible mechanisms.Method：A total of 54 SD rats were divided randomly into control group,SCI group （spinal cord injury group） and SCI followed MP treatment （MP group）.The SCI model in adult SD rats were built based on modified Allen＇s method. Mitochondria was extracted from injured spinal cord tissue by using modified Estabrook＇s method at 6h,12h and 24h prespectively after SCI.Then respiratory function index,including R3,R4,RCR,P/O and the contents of intramitochondria free calcium were measured.Result：R3,RCR and P/O in injured spinal cord mitochondria decreased significantly compared to the normal control group （P〈0.01） at 6h,12h and 24h after SCI,but the contents of intra mitochondria free calcium and R4 increased evidently（P〈0.01）.In MP group,R3,RCR and P/ O in injured spinal cord mitochondria significantly increased compared to SCI group（P〈0.01）,but the contents of intramitochondria free calcium and R4 decreased evidently （P 〈0.01）.There were significant difference between MP group and SCI group （P〈0.01）.Conclusion：The results suggest that mitochondrial respiratory function and the content of intramitochondria free calcium change significantly after SCI.Early administration of methylprednisolone could improve mitochondrial respiratory function while decrease the overload of intramitochondria free calcium in rats after SCI.