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Effect of Repeated Electroacupuncture Intervention on Hippocampal ERK and p38MAPK Signaling in Neuropathic Pain Rats

Results of our past studies showed that hippocampal muscarinic acetylcholine receptor (mAChR)-1 mRNA and differentially expressed proteins participating in MAPK signaling were involved in electroacupuncture (EA) induced cumulative analgesia in neuropathic pain rats, but the underlying intracellular...

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Detalles Bibliográficos
Autores principales: Wang, Jun-ying, Chen, Shu-ping, Gao, Yong-hui, Qiao, Li-na, Zhang, Jian-liang, Liu, Jun-ling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4487344/
https://www.ncbi.nlm.nih.gov/pubmed/26161123
http://dx.doi.org/10.1155/2015/641286
Descripción
Sumario:Results of our past studies showed that hippocampal muscarinic acetylcholine receptor (mAChR)-1 mRNA and differentially expressed proteins participating in MAPK signaling were involved in electroacupuncture (EA) induced cumulative analgesia in neuropathic pain rats, but the underlying intracellular mechanism remains unknown. The present study was designed to observe the effect of EA stimulation (EAS) on hippocampal extracellular signal-regulated kinases (ERK) and p38 MAPK signaling in rats with chronic constrictive injury (CCI) of the sciatic nerve, so as to reveal its related intracellular targets in pain relief. After CCI, the thermal pain thresholds of the affected hind were significantly decreased compared with the control group (P < 0.05). Following one and two weeks' EAS of ST 36-GB34, the pain thresholds were significantly upregulated (P < 0.05), and the effect of EA2W was remarkably superior to that of EA2D and EA1W (P < 0.05). Correspondingly, CCI-induced decreased expression levels of Ras, c-Raf, ERK1 and p-ERK1/2 proteins, and p38 MAPK mRNA and p-p38MAPK protein in the hippocampus tissues were reversed by EA2W (P < 0.05). The above mentioned results indicated that EA2W induced cumulative analgesic effect may be closely associated with its function in removing neuropathic pain induced suppression of intracellular ERK and p38MAPK signaling in the hippocampus.