Journal
NEUROCHEMISTRY INTERNATIONAL
Volume 75, Issue -, Pages 112-119Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuint.2014.05.012
Keywords
Diabetic neuropathy; Sodium channel; TNF-alpha; NF-kappa B; Dorsal root ganglia
Categories
Funding
- Natural Science Foundation of Guangdong [S2012040006843, S2013010011889]
- National Natural Science Foundation of China [30900436]
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Diabetic neuropathy (DN) is a common form of peripheral neuropathy, yet the mechanisms responsible for chronic pain in this disease are poorly understood. The up-regulation of the expression and function of voltage-gated sodium channel Nav1.7 has been implicated in DN, however, the exact mechanism is unclear. In the present study, we found that a proportion of streptozotocin (STZ)-treated rats suffered from mechanical allodynia and thermal hyperalgesia for a long-lasting time. Nav1.7 was up-regulated in spinal dorsal root ganglia (DRG) of rats with DN, double immunofluorescence staining showed that the increased Nav1.7 was co-localized with large and small sized neurons but not satellite glial cells. Inhibiting the synthesis of tumor necrosis factor-alpha (TNF-alpha) by thalidomide prevented DN, accompanied by strongly blocking the up-regulation of Nav1.7, TNF-alpha and p-nucleus factor-kappa B (p-NF-kappa B) in DRG. Intrathecal injection of NF-kappa B inhibitor pyrrolidine dithiocarbamate (PDTC) significantly attenuated the pain behaviors and over-expression of Nav1.7 in DRG neurons. These data suggest that increased TNF-alpha may be responsible for up-regulation of Nav1.7 in DRG neurons of rats with DN, and NF-kappa B signal pathway is involved in this process. The findings might provide potential target for preventing diabetic neuropathy. (C) 2014 Elsevier Ltd. All rights reserved.
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