重庆医学2018，Vol.47Issue(7)：868-870,874,4.DOI:10.3969/j.issn.1671-8348.2018.07.002
ASK1在大鼠脊髓损伤后炎症因子介导继发损伤中的机制研究
Study on mechanism of apoptosis signal regulating kinase 1 in inflammatory cytokine mediated secondary injury after spinal cord injury in rats
摘要
Abstract
Objective To explore the role of apoptosis signal regulating kinase 1(ASK1) in inflammatory mediated secondary injury after spinal cord injury(SCI) in rats.Methods The rat contusion SCI model was used.Forty-eight rats were randomly divided into the sham operation group(Sham),normal saline(Saline group) and inflammatory factors group (Cytokine group) respectively.The expressions of ASK1 and phosphorylated ASK1(pASK1) were detected by using Western blot.The Basso Beattie Bresnahan (BBB) scores and Grid Walking method were performed to assess the behavior changes of injured rat hindlimbs.Somatosensory evoked potential(SEP) and motor evoked potential(MEP) were used to examine the electrophysiological change.Results The expression levels of ASK1 mRNA and protein had no obvious change at 1 week after SCI;the pASK1 expression level in the Cytokine group was significantly up-regulated compared with the Saline group(P=0.002);the BBB scores at 3 or 4 weeks after SCI in the Cytokine group was significantly decreased compared with the Saline group (P =0.000,P =0.000);the hindlimbs missed step rate at 4 weeks following SCI in the Cytokine group was increased compared with the Saline group (P =0.032);the latent period of SEP and MEP in the Cytokine group was prolonged(P =0.043,P =0.045),while the wave peak value had no obvious changed (P =0.889,P=0.434).Conclusion Inflammatory cytokines may lead the hindlimbs movement dysfunction to be aggravated after SCI in rat,its mechanism may be related with the phosphorylation elevation of ASK1.关键词
脊髓损伤/大鼠/细胞凋亡信号调节蛋白1/炎症细胞因子Key words
spinal cord injury/rats/apoptosis signal regulating kinase 1/inflammatory cytokine分类
医药卫生引用本文复制引用
夏永智,黎天尊,廖正步,夏海坚,晏怡..ASK1在大鼠脊髓损伤后炎症因子介导继发损伤中的机制研究[J].重庆医学,2018,47(7):868-870,874,4.基金项目
国家自然科学基金资助项目(81100906) （81100906）
国家临床重点专科建设项目经费(财社[2011]170号). （财社[2011]170号）
