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 Journal of Andrology
;
(6): 300-305, 2018.
Artigo
em Inglês
| WPRIM
| ID: wpr-1009561
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.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Dor
/
Peptídeos
/
Fosforilação
/
Prostatite
/
Piridinas
/
Venenos de Aranha
/
Regulação para Cima
/
Quelantes
/
Cálcio
/
Doença Crônica
Limite:
Animais
Idioma:
Inglês
Revista:
Asian Journal of Andrology
Ano de publicação:
2018
Tipo de documento:
Artigo
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