[Aim] Lower urinary tract symptoms due to intrapelvic nerves damage are frequent complications of pelvic surgery. Previously, we reported that bilateral injury to accessory nerves (ACN), which extend from the major pelvic ganglion, resulted in bladder fibrosis and bladder dysfunction in rats within 72 h until at least 4 weeks post-surgery. Prevention of bladder fibrosis is necessary to maintain bladder function. Herein, we examined the mechanisms underlying bladder fibrosis associated with ACN injury.
[Methods] Ten-week-old male Wistar/ST rats were categorized into sham and bilateral ACN injury (BAI) groups. In the BAI group, the ACN was crushed for 1 min using reverse-action tweezers on both sides. After 4, 8, 12, 24, and 72 h, we examined bladder histology using Masson‘s trichrome staining and evaluated mRNA expression levels of TGF-β1 and MCP-1 using real-time PCR analysis.
[Results] Increased collagen area-to-total bladder area ratio of BAI groups was noted at 12, 24, and 72 h postoperatively, compared to sham groups. Postoperative mRNA expression levels of TGF-β1 and MCP-1 at 12, 24, and 72 h, and 4, 8, 12, and 24 h respectively, were higher in BAI groups compared to sham groups.
[Conclusion] Upregulation of MCP-1 followed by TGF-β1 may be involved in bladder fibrosis associated with ACN injury.