大鼠脊髓缺血再灌注损伤后NF-κB的表达及异丙酚的影响  

The expression of NF-Kappa B in spinal cord ischemia-reperfusion injury and the protective action of propofol in rat

作　　者：罗风芹[1] 周青山[1] 刘先义[1] 夏中元[1] 杜大平[1] 

机构地区：[1]武汉大学人民医院麻醉科,430060

出　　处：《卒中与神经疾病》2005年第1期14-16,27,共4页Stroke and Nervous Diseases

摘　　要：目的　探讨异丙酚对大鼠脊髓缺血再灌注损伤后NF κB的表达及神经元凋亡的影响。方法　成年大鼠随机分为脊髓缺血后异丙酚治疗组(P组)和单纯缺血再灌注组(Ⅰ组),建立脊髓缺血再灌注模型,脊髓神经元NF κB亚单位水平通过免疫组化来测定,用HE染色观察脊髓组织病理学变化,原位末端标记法(TUNEL法)标记凋亡细胞。结果　HE染色镜检发现脊髓组织病理学改变P组明显轻于Ⅰ组;Ⅰ组脊髓神经元P65亚单位的表达较P组显著增强(P<0.01);P组脊髓神经元凋亡较Ⅰ组明显减少(P<0.01)。结论　脊髓缺血再灌注可导致NF κB表达增多,凋亡神经元增多;NF κB的激活与神经元凋亡相关;异丙酚可抑制脊髓神经元NF κB的表达,减少神经元凋亡。Objective To investigate the effect of propofol on expression of NF κB and apoptosis after spinal cord ischemia reperfusion (1/R)in rats.Methods Experimental rats were divided into two groups:propofol protecting group (group P),and ischmian reperfusion group (group Ⅰ).Spinal cord ischemia reperfusion model was prepared in adult male rats by abdominal artery occlusion.The histopathological changes in spinal cord were abservred by hematoxylin and eosion (HE)staining.The expression of NF κ BP65 subunit was measured by immunohistochemistry and the apopotosis of spinal cord neurons was examined by the terminal deoxynucleotidal transferase mediated DUTP biotin nick end labeling (TUNEL) reaction.Results The histopathological changes in group Ⅰ were obviously greater than that in group P and the apopototic index and expression of NF κ BP65 subunit in group Ⅰ were stronger than those in group P( P < 0.01 ).Conclusions Transient ischemia induce a marked activation of NF κ B and notable evidence of apopotosis in the neurons of spinal cord.The activation of NF κ B was associated with apopotosis of neurons.The results suggest that propofol may inhibit neuronal apopotosis by preventing the activation of NF κ B.

关 键 词：脊髓 凋亡 核因子KB 异丙酚 缺血再灌注 

分 类 号：R744[医药卫生—神经病学与精神病学]