Open Access

Mechanisms of autophagy and apoptosis mediated by JAK2 signaling pathway after spinal cord injury of rats

  • Authors:
    • Yongzhi Xia
    • Haijian Xia
    • Dan Chen
    • Zhengbu Liao
    • Yi Yan
  • View Affiliations

  • Published online on: June 26, 2017     https://doi.org/10.3892/etm.2017.4674
  • Pages: 1589-1593
  • Copyright: © Xia et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

The aim of this study was to investigate the pathogenesis of autophagy and apoptosis mediated by Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signal pathway after the onset of acute spinal cord injury (ASCI). A total of 45 Sprague-Dawley adult rats of either sex were selected for this study. The age of rats ranged from 8 to 10 weeks, and the average weight was 245 g. These rats were randomly divided into three groups, i.e. sham-operated group, model group, and the AG-490 intervention group (AG-490 is an inhibitor of JAK2). Each group contained 15 rats. Models were prepared using the modified Allen method. Five rats in each group were sacrificed at 6, 12 and 24 h, respectively, and the expression levels of p-JAK2 and p-STAT3 were detected in spinal cord tissue via western blot analysis. The levels of proinflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected via ELISA, positive expression of light chain 3 (LC3)-II of microtubule-associated protein 1 via immunofluorescence labeling method, and mRNA expression levels of caspase-3 and Bax/Bcl-2 via RT-PCR. In the model group, the expression levels of p-JAK2, p-STAT3, IL-6, TNF-α and LC3-II, and the mRNA expression levels of caspase-3 and Bax/Bcl-2 at all time-points were significantly higher than those in the AG-490 intervention group, and the levels in the sham-operated group were the lowest (p<0.05). In the model group, peak levels of p-JAK2 and p-STAT3 were attained at 12 h, but a decline was seen at 24 h; while increasing trend was seen in other indicators. In conclusion, JAK2/STAT3 signal pathway can mediate the activity of autophagy and apoptosis in an early stage after the onset of ASCI of rat.
View Figures
View References

Related Articles

Journal Cover

August-2017
Volume 14 Issue 2

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Xia Y, Xia H, Chen D, Liao Z and Yan Y: Mechanisms of autophagy and apoptosis mediated by JAK2 signaling pathway after spinal cord injury of rats. Exp Ther Med 14: 1589-1593, 2017
APA
Xia, Y., Xia, H., Chen, D., Liao, Z., & Yan, Y. (2017). Mechanisms of autophagy and apoptosis mediated by JAK2 signaling pathway after spinal cord injury of rats. Experimental and Therapeutic Medicine, 14, 1589-1593. https://doi.org/10.3892/etm.2017.4674
MLA
Xia, Y., Xia, H., Chen, D., Liao, Z., Yan, Y."Mechanisms of autophagy and apoptosis mediated by JAK2 signaling pathway after spinal cord injury of rats". Experimental and Therapeutic Medicine 14.2 (2017): 1589-1593.
Chicago
Xia, Y., Xia, H., Chen, D., Liao, Z., Yan, Y."Mechanisms of autophagy and apoptosis mediated by JAK2 signaling pathway after spinal cord injury of rats". Experimental and Therapeutic Medicine 14, no. 2 (2017): 1589-1593. https://doi.org/10.3892/etm.2017.4674