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Involvement of the Sodium Channel Nav1.7 in Paclitaxel-induced Peripheral Neuropathy through ERK1/2 Signaling in Rats

[ Vol. 17 , Issue. 3 ]

Author(s):

Guang Jie Wang, Xi Zhang, Li-De Huang and Yun Xiao*   Pages 267 - 274 ( 8 )

Abstract:


Background: Paclitaxel treatment is a major cause of chemotherapy-induced peripheral neuropathy. The sodium channel Nav1.7 plays a critical role in pain perception. However, whether Nav1.7 in the dorsal root ganglion (DRG) is involved in paclitaxel-induced peripheral neuropathy remains unclear. Thus, our study aimed to evaluate whether Nav1.7 participates in the pathogenesis of paclitaxel-induced neuropathy.

Methods: Paclitaxel-induced peripheral neuropathy was generated by intraperitoneal administration of paclitaxel on four alternate days.

Results: The results showed that DRG mRNA and protein expression levels of Nav1.7 were upregulated between days 7 and 21 after the administration of paclitaxel. Besides, paclitaxel upregulated extracellular signal-regulated kinase (ERK1/2) phosphorylation in DRG. Intrathecal injection of U0126 (a MEK inhibitor) blocking ERK1/2 phosphorylation blunted up-regulation of Nav1.7 in the DRG and correspondingly attenuated hyperalgesia.

Conclusion: These results indicated that the sodium channel Nav1.7 in the DRG exerted an important function in paclitaxel-induced neuropathy, which was associated with ERK phosphorylation in neurons.

Keywords:

Extracellular signal-regulated kinase, dorsal root ganglion, hyperalgesia, paclitaxel-induced peripheral neuropathy, neuron, chemotherapeutic drug.

Affiliation:

Department of Anesthesiology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, Department of Anesthesiology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, Department of Anesthesiology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, Department of Anesthesiology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000



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