The Influence of p38 Mitogen-Activated Protein Kinase Inhibitor on Synthesis of Inflammatory Cytokine Tumor Necrosis Factor Alpha in Spinal Cord of Rats with Chronic Constriction Injury

Xu, Li; Huang, Yuguang; Yu, Xuerong; Yue, Jianying; Yang, Nan; Zuo, Pingping

doi:10.1213/01.ane.0000287660.29297.7b

Cited by 50 publications

(44 citation statements)

References 25 publications

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“…Activated p38 in DRG and spinal cord was transiently elevated after SnL and then recovered to basal levels 25 . Xu 26 , Lee 28 and present data indicate that activated p38 in spinal cord elevated after CCI and sustained for 14 days and more. Differences among the various models seem to cause substantial differences in spinal p38 activation.…”

Section: Discussionsupporting

confidence: 64%

Melanocortin 4 Receptor Mediates Neuropathic Pain Through p38MAPK in Spinal Cord

Xia

et al. 2012

Can. J. Neurol. Sci.

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458Peripheral nerve injury often results in neuropathic pain associated with hyperalgesia and allodynia 1 . Several lines of evidence suggest that melanocortin 4 receptor (MC4R) plays an important role in the initiation of neuropathic pain. MC4R is activated after nerve injury. Intraplantar injection of MC4 receptor antagonists can abolish chronic constriction injury (CCI)-induced allodynia and hyperalgesia 2 . It suggests that MC4R is involved in the transduction of neuropathic pain. Recently MC4R was found in dorsal root ganglia (DRG) where nerve injury can affect its expression 3 , but the underlying mechanisms are still unclear. P38MAPK was improved to play an important role in the development and maintenance of nerve injury, inflammation and incision pain [4][5][6][7][8][9] . Intrathecal inhibitor of p38 has been shown to attenuate neuropathic pain in different ABSTRACT: Background: neuropathic pain is characterised by spontaneous ongoing or shooting pain and evoked amplified pain responses after noxious or non-noxious stimuli. neuropathic pain develops as a result of lesions or disease affecting the somatosensory nervous system either in the periphery or centrally. Melanocortin 4 receptor (MC4R) plays an important role in the initiation of neuropathic pain but the underlying mechanisms are still unclear. Methods: Adult male Wistar rats were given chronic constriction injury (CCI) or sham operations. Part of CCI rats were intrathecally treated with HS014 (MC4R antagonist) or Sb203580 (p38MAPK inhibitor). on the third, seventh and fourteenth day, the thermal threshold of operated paws was tested. In addition, the MC4R or phosphorylated p38MAPK (p-p38MAPK) levels of lumbar spinal cord were tested with eLISA（enzyme-linked immunosorbent assay), western blot and immunohistochemistry. Results: Here we demonstrate that (1) both HS014 and Sb203580 reduced CCI reduced hyperalgesia (2) p-p38MAPK was increased after CCI with a time course parallel to that of the MC4R change, (3) The p38 activation was prevented by blocking MC4R with an antagonist HS014, but MC4R-IR was not prevented by Sb203580. (4) MC4R and pp38MAPK were located in the same cells. Conclusion: The mechanisms of neuropathic pain mediated by MC4R is related to the inhibition of p38MAPK activation.P38MAPK may be a downstream of MC4R. RÉSUMÉ: Médiation de la douleur neuropathique par le récepteur de la mélanocortine 4 par l'entremise de p38MAPK dans la moelle épinière. Contexte : La douleur neuropathique est caractérisée par une douleur spontanée persistante ou lancinante et des réponses douloureuses amplifiées évoquées suite à des stimuli, qu'ils soient nocifs ou non. La douleur neuropathique apparaît suite à des lésions ou à une maladie qui touche le système nerveux somatosensitif périphérique ou central. Le récepteur de la mélanocortine 4 (MC4R) joue un rôle important dans la genèse de la douleur neuropathique. Les mécanismes sous-jacents demeurent cependant mal connus. Méthode : Des rats Wistar mâles adultes ont subi une lésion par constriction chroni...

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Section: Discussionsupporting

confidence: 64%

Melanocortin 4 Receptor Mediates Neuropathic Pain Through p38MAPK in Spinal Cord

Xia

et al. 2012

Can. J. Neurol. Sci.

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“…Accumulating evidence shows that MAPKs mediate the production of a variety of proinflammatory cytokines and chemokines in glial cells (Gao et al, 2009;Lu et al, 2013;Xu et al, 2007). Our previous results showed that the protein expression of MCP-1 was regulated by JNK and ERK pathway in astrocytes (Gao et al, 2009).…”

Section: Ho-1 Induction Reduces Activation Of Mapks and Production Ofmentioning

confidence: 86%

Exogenous induction of HO-1 alleviates vincristine-induced neuropathic pain by reducing spinal glial activation in mice

Yan

Zhang

Zhu

et al. 2015

Neurobiology of Disease

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“…7 Moreover, Ang-(1-7) binding to MasR may inhibit phosphorylation of p38 MAPK. 41 Phosphorylation of spinal p38 MAPK has been observed in chronic injury, 77 and therefore a decrease in phospho-p38 MAPK in chronic injury models such as CIBP may prove to yield antinociceptive effect. MasR activation by Ang-(1-7) can activate nitric oxide synthase, increasing intracellular NO 8 to further increase intracellular levels of cyclic GMP (cGMP).…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-(1-7)/Mas receptor as an antinociceptive agent in cancer-induced bone pain

Forte

Slosky

Zhang

et al. 2016

Pain

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The Influence of p38 Mitogen-Activated Protein Kinase Inhibitor on Synthesis of Inflammatory Cytokine Tumor Necrosis Factor Alpha in Spinal Cord of Rats with Chronic Constriction Injury

Abstract: p38 MAPK activation is one aspect of the signaling cascade that culminates in TNF-alpha synthesis and contributes to mechanical allodynia after peripheral nerve injury.

Cited by 50 publications

References 25 publications

Melanocortin 4 Receptor Mediates Neuropathic Pain Through p38MAPK in Spinal Cord

Melanocortin 4 Receptor Mediates Neuropathic Pain Through p38MAPK in Spinal Cord

Exogenous induction of HO-1 alleviates vincristine-induced neuropathic pain by reducing spinal glial activation in mice

Angiotensin-(1-7)/Mas receptor as an antinociceptive agent in cancer-induced bone pain

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