Spinal CXCL5 contributes to nerve injury-induced neuropathic pain via modulating GSK-3β phosphorylation and activity in rats
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- 作者：Weituan Xu ; Min Zhu ; Shaoting Yuan ; Wenli Yu ; yzxmzkywl@126.com" class="auth_mail" title="E-mail the corresponding author
- 关键词：CCI ; chronic constriction injury ; CXCL5 ; chemokine (CXC motif) ligand 5 ; GAPDH ; glyceraldehydes 3-phosphate dehydrogenase ; GSK-3β ; glycogen synthase kinase-3β ; NMDA ; N-methyl-d-aspartate ; NS ; normal saline ; PWL ; paw withdrawal thermal latency ; PWT ; paw withdrawal mechanical threshold ; SD ; standard deviation
- 刊名：Neuroscience Letters
- 出版年：2016
- 出版时间：10 November 2016
- 年：2016
- 卷：634
- 期：Complete
- 页码：52-59
- 全文大小：2145 K
文摘
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CCI-induced postoperative mechanical allodynia and thermal hyperalgesia.
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Up-regulation of CXCL5 and CXCR2 expression and GSK-3β activity in spinal dorsal horn after CCI treatment.
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Intrathecal blockage of CXCL5/CXCR2 effectively ameliorated CCI-induced neuropathic pain.
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CXCL5/CXCR2 inhibition down-regulated spinal GSK-3β activity in CCI-induced neuropathic pain.
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Intrathecal delivery of CXCL5 induced pain hypersensitivity, which was attenuated by GSK-3β inhibitor.
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