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Correlation of TGN-020 With the Analgesic Effects via ERK Pathway Activation After Chronic Constriction Injury

Correlation of TGN-020 With the Analgesic Effects via ERK Pathway Activation After Chronic Constriction Injury

Liang Zhao, Dan Li, Nan Liu, Lu Liu, Zhuo Zhang, Chao Gao, Hitoshi Kawano, Fang-Yuan Zhou, Hong-Peng Li

Mol Pain. Jan-Dec 2018;14:1744806918796057.

PMID: 30152258

Abstract:

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-1β, interleukin-6, and tumor necrosis factor-α, 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.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP51987996	TGN-020		51987-99-6	Price

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