ORIGINAL ARTICLE
Year : 2018  |  Volume : 20  |  Issue : 3  |  Page : 300-305

ASIC1a contributes to the symptom of pain in a rat model of chronic prostatitis


1 Department of Urology, Institute of Urology, Anhui Medical University, Hefei 230022, China
2 The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China

Correspondence Address:
Dr. Chao-Zhao Liang
Department of Urology, Institute of Urology, Anhui Medical University, Hefei 230022, China; The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/aja.aja_55_17

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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.


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