ASIC1a contributes to the symptom of pain in a rat model of chronic prostatitis.
- Author:
Song FAN
1
;
Zong-Yao HAO
1
;
Li ZHANG
1
;
Jun ZHOU
1
;
Yi-Fei ZHANG
1
;
Shen TAI
1
;
Xian-Sheng ZHANG
1
;
Chao-Zhao LIANG
1
Author Information
- Publication Type:Journal Article
- Keywords: ASIC1a; chronic prostatitis; pain symptom
- MeSH: Acid Sensing Ion Channel Blockers/pharmacology*; Acid Sensing Ion Channels/genetics*; Animals; Calcium/metabolism*; Chelating Agents/pharmacology*; Chronic Disease; Cytokines/metabolism*; Disease Models, Animal; Egtazic Acid/pharmacology*; Gene Knockdown Techniques; Imidazoles/pharmacology*; Inflammation/metabolism*; MAP Kinase Signaling System/genetics*; Male; Pain/genetics*; Peptides/pharmacology*; Phosphorylation/drug effects*; Posterior Horn Cells/metabolism*; Prostatitis/complications*; Protein Kinase Inhibitors/pharmacology*; Pyridines/pharmacology*; Rats; Spider Venoms/pharmacology*; Up-Regulation; p38 Mitogen-Activated Protein Kinases/metabolism*
- From: Asian Journal of Andrology 2018;20(3):300-305
- CountryChina
- Language:English
- 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.
