Study on mechanism of apoptosis signal regulating kinase 1 in inflammatory cytokine mediated secondary injury after spinal cord injury in rats
10.3969/j.issn.1671-8348.2018.07.002
- VernacularTitle: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
- Author:
Yongzhi XIA
1
;
Tianzun LI
;
Zhengbu LIAO
;
Haijian XIA
;
Yi YAN
Author Information
1. 重庆医科大学附属第一医院神经外科 400016
- Keywords:
spinal cord injury;
rats;
apoptosis signal regulating kinase 1;
inflammatory cytokine
- From:
Chongqing Medicine
2018;47(7):868-870,874
- CountryChina
- Language:Chinese
-
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.
