Objective: To investigate the expression of type 3 acid-sensing ion channels (ASIC3) in bladder tissue of over active bladder (OAB) rat model.
Methods: Sixty adult female rats were randomly divided into control group (intraperitoneal injection of 0.9% sodium chloride), GAB group (intraperitoneal injection of cyclophosphamide) and the intervention group (OAB rats treated with ASIC3 inhibitor amiloride). The rats underwent urodynamic testing. The bladder tissues were collected for pathological examination, while the expressions of ASIC3 were measured by the methods of immunohistochemistry, RT-PCR and Western blot.
Results: Urodynamic study found that the rats in control group had no significant contraction instability in both storage and voiding stages. Compared with the control group, OAB group and intervention group showed instability of visible contraction in urine storage stage, with shorter micturition interval (P < 0.01) and increased frequency of urination (P < 0.01). Compared with the OAB group, the intervention group showed significantly prolonged micturition interval (P < 0.05) and reduced frequency of urination (P < 0.05). Pathologic examination showed rat bladder mucosal damage in both OAB group and intervention group. Immunohistochemistry found the expression of ASIC3 on bladder mucosa. RT-PCR and Western blot showed significantly higher expression of ASIC3 in OAB group (P < 0.01), but the expression of ASIC3 decreased in intervention group after adding ASIC3 inhibitor. CONCLUSION ASIC3 expresses mainly on bladder mucosa. The gene and protein expression of ASIC3 in rat bladder tissue of OAB rats is higher, which can be significantly decreased by ASIC inhibitor. The symptoms of OAB reduce after intervention, which demonstrates the increased expression of ASIC3 in bladder tissue is closely related to bladder detrusor.