ASIC1a contributes to the symptom of pain in a rat model of chronic prostatitis / 亚洲男科学杂志(英文版)
Asian j. androl
; Asian j. androl;(6): 300-305, 2018.
Article
de En
| WPRIM
| ID: wpr-1009561
Bibliothèque responsable:
WPRO
ABSTRACT
This study aims to validate our hypothesis that acid-sensing ion channels (ASICs) may contribute to the symptom of pain in patients with chronic prostatitis (CP). We first established a CP rat model, then isolated the L5-S2 spinal dorsal horn neurons for further studies. ASIC1a was knocked down and its effects on the expression of neurogenic inflammation-related factors in the dorsal horn neurons of rat spinal cord were evaluated. The effect of ASIC1a on the Ca2+ ion concentration in the dorsal horn neurons of rat spinal cord was measured by the intracellular calcium ([Ca2+]i) intensity. The effect of ASIC1a on the p38/mitogen-activated protein kinase (MAPK) signaling pathway was also determined. ASIC1a was significantly upregulated in the CP rat model as compared with control rats. Acid-induced ASIC1a expression increased [Ca2+]i intensity in the dorsal horn neurons of rat spinal cord. ASIC1a also increased the levels of neurogenic inflammation-related factors and p-p38 expression in the acid-treated dorsal horn neurons. Notably, ASIC1a knockdown significantly decreased the expression of pro-inflammatory cytokines. Furthermore, the levels of p-p38 and pro-inflammatory cytokines in acid-treated dorsal horn neurons were significantly decreased in the presence of PcTx-1, BAPTA-AM, or SB203580. Our results showed that ASIC1a may contribute to the symptom of pain in patients with CP, at least partially, by regulating the p38/MAPK signaling pathway.
Mots clés
Texte intégral:
1
Indice:
WPRIM
Sujet Principal:
Douleur
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Peptides
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Phosphorylation
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Prostatite
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Pyridines
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Venins d'araignée
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Régulation positive
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Chélateurs
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Calcium
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Maladie chronique
Limites du sujet:
Animals
langue:
En
Texte intégral:
Asian j. androl
Année:
2018
Type:
Article