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 p38lmitogen-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.