Effects of Prolyl 4-Hydroxylase Inhibitor on Bladder Function, Bladder Hypertrophy and Collagen Subtypes in a Rat Model With Partial Bladder Outlet Obstruction

Objective To investigate the effects of prolyl 4-hydroxylase (P4H) inhibitor on the bladder in rats with partial bladder outlet obstruction. Methods Forty-five female Sprague–Dawley rats were divided into 3 groups; partial bladder outlet obstruction with P4H inhibitor 20 mg/kg (groups A1, A2, and A4, each n = 5), partial bladder outlet obstruction with normal saline (groups B1, B2, and B4, each n = 5), and normal control (groups C1, C2, and C4, each n = 5). After partial bladder outlet obstruction for 1, 2, and 4 weeks in the groups A and B, respectively, the inhibitor or normal saline were administered orally at the indicated dosage once a day for 2 weeks. After either 3, 4, or 6 weeks, the bladders were removed after cystometry. Results The pressure and volume parameters from the cystometry and the muscle thickness from the Masson trichrome staining of groups A and B increased significantly compared to those in group C (P < .05), and those in group A were significantly lower than those of group B (P < .05). Based on immunohistochemical staining and reverse transcription-polymerase chain reaction, P4H expression in groups A and B was increased compared with that in group C. Furthermore, P4H expression showed a larger decrease in group A compared to that in group B. Collagens I and III protein expressions increased with partial bladder outlet obstruction in comparison with that of group C, and expression in group A was marginally decreased compared with expression in group B. Conclusion Our data suggest that the P4H inhibitor may improve bladder function and reduce the bladder fibrosis caused by partial bladder outlet obstruction. To investigate the effects of prolyl 4-hydroxylase (P4H) inhibitor on the bladder in rats with partial bladder outlet obstruction. Forty-five female Sprague–Dawley rats were divided into 3 groups; partial bladder outlet obstruction with P4H inhibitor 20 mg/kg (groups A1, A2, and A4, each n = 5), partial bladder outlet obstruction with normal saline (groups B1, B2, and B4, each n = 5), and normal control (groups C1, C2, and C4, each n = 5). After partial bladder outlet obstruction for 1, 2, and 4 weeks in the groups A and B, respectively, the inhibitor or normal saline were administered orally at the indicated dosage once a day for 2 weeks. After either 3, 4, or 6 weeks, the bladders were removed after cystometry. The pressure and volume parameters from the cystometry and the muscle thickness from the Masson trichrome staining of groups A and B increased significantly compared to those in group C (P < .05), and those in group A were significantly lower than those of group B (P < .05). Based on immunohistochemical staining and reverse transcription-polymerase chain reaction, P4H expression in groups A and B was increased compared with that in group C. Furthermore, P4H expression showed a larger decrease in group A compared to that in group B. Collagens I and III protein expressions increased with partial bladder outlet obstruction in comparison with that of group C, and expression in group A was marginally decreased compared with expression in group B. Our data suggest that the P4H inhibitor may improve bladder function and reduce the bladder fibrosis caused by partial bladder outlet obstruction.