Journal
MOLECULAR PAIN
Volume 14, Issue -, Pages -Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/1744806918796057
Keywords
Neuropathic pain; chronic constriction injury; ERK pathway; astrocyte activation; inflammatory
Categories
Funding
- National Natural Science Foundation of China (NSFC) [NSFC-81171248]
- Liaoning Provincial Department of Education fund [LZDK-201704]
Ask authors/readers for more resources
Extracellular regulated protein kinase (ERK) pathway activation in astrocytes and neurons has been reported to be critical for neuropathic pain development after chronic constriction injury. TGN-020 was found to be the most potent aquaporin 4 inhibitor among the agents studied. The present study aimed to assess whether the inhibition of aquaporin 4 had an analgesic effect on neuropathic pain and whether the inhibition of astrocytic activation and ERK pathway was involved in the analgesic effect of TGN-020. We thus found that TGN-020 upregulated the threshold of thermal and mechanical allodynia, downregulated the expression of interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha, attenuated the astrocytic activation and suppressed the activation of mitogen-activated protein kinase pathways in the spinal dorsal horn and dorsal root ganglion. Additionally, TGN-020 suppressed ERK phosphorylation in astrocytes and neurons after injury. The findings suggested that the analgesic effects of TGN-020 in neuropathic pain were mediated mainly by the downregulation of chronic constriction injury-induced astrocytic activation and inflammation, which is via the inhibition of ERK pathway in the spinal dorsal horn and dorsal root ganglion.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available