4.4 Article

Fucoidan attenuates the existing allodynia and hyperalgesia in a rat model of neuropathic pain

期刊

NEUROSCIENCE LETTERS
卷 571, 期 -, 页码 66-71

出版社

ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2014.04.030

关键词

Fucoidan; Neuropathic pain; Neuroimmune activation

资金

  1. Doctoral Program of Guangdong Medical College, China [XB1021]
  2. Science and Technology Project Foundation of Zhanjiang City, China [2010C3104009]
  3. Medical Scientific Research Foundation of Guangdong Province, China [B2010234]
  4. Breeding Project of the Education Department of Guangdong Province, China [LYM10084]

向作者/读者索取更多资源

Fucoidan is an active constituent found in brown seaweeds, which have potential neuroprotection. The current study aimed to investigate the effects of fucoidan on the maintenance of neuropathic pain induced by L5 spinal nerve ligation (SNL) and the underlying mechanism related to the spinal neuroimmune responses. Animals were randomized into 5 groups: sham-operation with vehicle and SNL with vehicle or fucoidan (15,50, and 100 mg/kg). Different doses of fucoidan or vehicle were administered intrathecally once daily from postoperative day (POD) 11-20. Mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) was measured on 1 day before operation and days 10, 20, 22, 24, 26, 28, 30 after operation. Glial activation markers such as glial fibrillary acidic protein (GFAP) and macrophage antigen complex-1 (mac-1), inflammatory cytokines such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta and IL-6 activation, and extracellular signalregulated protein kinase (ERK) activation in the lumbar spinal cord were determined on day 30 after operation. The results showed that fucoidan caused dose-dependently attenuation of mechanical allodynia and thermal hyperalgesia. Furthermore, fucoidan could markedly inhibit neuroimmune activation characterized by glial activation, production of cytokines as well as ERK activation. The analgesic effect of intrathecal fucoidan in rats receiving SNL might partly attribute to the inhibition of neuroimmune activation associated with the maintenance of neuropathic pain. (C) 2014 The Authors. Published by Elsevier Ireland Ltd.

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