摘要
目的观察p62、核因子κB(NF-κB)以及caspase-3在大鼠脊髓损伤中的表达,并探讨相关机制。方法60只大鼠随机分为假手术组和实验组,实验组大鼠采用Allen法制作脊髓损伤模型,分别于24 h、48 h和72 h进行神经功能评分,以及通过Western blot法检测不同时间段p62和NF-κB蛋白表达,Elisa法检测不同时间段caspase-3蛋白水平。结果脊髓损伤后大鼠BBB评分显著降低,并随造模时间的延长而上升(P<0.05),Western blot法显示脊髓损伤后p62和NF-κB蛋白水平明显提高,而随时间的延长p62和NF-κB蛋白表达下降(P<0.05),Elisa法显示脊髓损伤后caspase-3活性明显提高,而随时间的延长caspase-3蛋白活性得到显著下降(P<0.05)。结论脊髓损伤可激活p62与NF-κB介导的凋亡通路,并对损伤脊髓的细胞凋亡起着重要的调控作用。
Objective To explore the molecular mechanism of p62/NF-κB-mediated apoptosis pathway in acute spinal cord injury in rats.Methods 60 SD rats were divided into 2 groups： Sham group and test group.The spinal cord injury was established via Allen method,and neurological function in the test group was valued at 24 h,48 h and 72 h.and the relative protein expression of p62 and NF-κB were detected by western blot.Caspase-3 activity was detected by elisa.Results BBB score was significantly decreased in the spinal cord injury mice,and rised with time.Meanwhile,the protein expression of p62 and NF-κB were increased in the spinal cord injury mice,and the expression of p62 and NF-κB protein decreased with time.Elisa showed that the activity of caspase-3 was markedly increased and decreased with time.Conclusion p62/NF-κB-mediated apoptosis pathway was activated in acute spinal cord injury.
出处
《临床和实验医学杂志》
2017年第13期1255-1258,共4页
Journal of Clinical and Experimental Medicine
