Behavioral evidence for the differential regulation of p-p38 MAPK and p-NF-κB in rats with trigeminal neuropathic painReport as inadecuate




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Molecular Pain

, 7:57

First Online: 05 August 2011Received: 11 June 2011Accepted: 05 August 2011

Abstract

BackgroundWe investigated the differential regulation of p-p38 MAPK or p-NF-κB in male Sprague-Dawley rats with inferior alveolar nerve injury resulting from mal-positioned dental implants. For this purpose, we characterized the temporal expression of p-p38 MAPK or p-NF-κB in the medullary dorsal horn and examined changes in nociceptive behavior after a blockade of p-p38 MAPK or p-NF-κB pathways in rats with trigeminal neuropathic pain.

ResultsUnder anesthesia, the left lower second molar was extracted and replaced with a mini dental implant to intentionally injure the inferior alveolar nerve. Western and immunofluorescence analysis revealed that p-p38 MAPK is upregulated in microglia following nerve injury and that this expression peaked on postoperative day POD 3 through 7. However, the activation of p-NF-κB in astrocyte peaked on POD 7 through 21. The intracisternal administration of SB203580 1 or 10 μg, a p38 MAPK inhibitor, on POD 3 but not on POD 21 markedly inhibits mechanical allodynia and the p-p38 MAPK expression. However, the intracisternal administration of SN50 0.2 or 2 ng, an NF-κB inhibitor, on POD 21 but not on POD 3 attenuates mechanical allodynia and p-NF-κB expression. Dexamethasone 25 mg-kg decreases not only the activation of p38 MAPK but also that of NF-κB on POD 7.

ConclusionsThese results suggest that early expression of p-p38 MAPK in the microglia and late induction of p-NF-κB in astrocyte play an important role in trigeminal neuropathic pain and that a blockade of p-p38 MAPK at an early stage and p-NF-κB at a late stage might be a potential therapeutic strategy for treatment of trigeminal neuropathic pain.

Abbreviationsp-p38 MAPKphospho-p38 mitogen-activated protein kinase

p-NF-κBphospho-nuclear factor- kappa B

IL-1βinterleukin-1 beta

IL6interleukin-6

TNF-αtumor necrosis factor-alpha

PODpostoperative day

NeuNneuronal nuclei

GFAPglial fibrillary acidic protein

PBphosphate buffer

GAPDHGlyceraldehyde-3-phosphate dehydrogenase.

Electronic supplementary materialThe online version of this article doi:10.1186-1744-8069-7-57 contains supplementary material, which is available to authorized users.

Min K Lee, Seung R Han contributed equally to this work.

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Author: Min K Lee - Seung R Han - Min K Park - Min J Kim - Yong C Bae - Sung K Kim - Jae S Park - Dong K Ahn

Source: https://link.springer.com/







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