# Platelet-rich plasma improves cyclophosphamide-induced interstitial cystitis in rat models through the toll-like receptor 4/nuclear factor-kappa B signalling pathway

## TL;DR

Platelet-rich plasma (PRP) helps treat bladder inflammation in rats by improving epithelial function and reducing inflammation through a specific signaling pathway.

## Contribution

PRP's therapeutic effect on interstitial cystitis is linked to the TLR4/NF-κB pathway and improved epithelial integrity.

## Key findings

- PRP reduced inflammation and histological damage in cyclophosphamide-induced bladder inflammation in rats.
- PRP upregulated ZO-1, a marker of epithelial integrity, in bladder tissue and LPS-induced cells.
- PRP modulated the TLR4/NF-κB signaling pathway to alleviate mucosal injury in interstitial cystitis.

## Abstract

To investigate the therapeutic effect of platelet-rich plasma (PRP) on a cyclophosphamide (CYP)-induced interstitial cystitis (IC) rat model.

A CYP-induced IC rat model (75 mg/kg every 3 days, with a total of five injections) was used to evaluate the therapeutic effects of PRP. Here, PRP was administered via bladder irrigation (every 2 days, with a total of three irrigations), and bladder tissue was analysed for inflammation and histological changes. The toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) signalling pathway was assessed using real-time quantitative polymerase chain reaction and ribonucleic acid sequencing. In addition, lipopolysaccharide (LPS)-induced SV-HUC-1 cells (10 μg/LPS and 2.5 mM adenosine triphosphate) were employed to investigate the inflammatory response and the effects of PRP on the TLR4/NF-κB signalling pathway.

The PRP treatment significantly improved the bladder tissue condition in the CYP-induced IC rat model, as evidenced by reduced inflammation and histological damage. The damage and shedding of the superficial epithelium of the bladder mucosa were notably decreased following PRP bladder instillation. Importantly, the expression of ZO-1, a key marker of epithelial integrity, was upregulated in PRP-treated rats, indicating enhanced bladder epithelial function. High-throughput analysis revealed that PRP alleviated bladder mucosal injury in the IC rat model through the TLR4/NF-κB signalling pathway. In LPS-induced SV-HUC-1 cells, PRP treatment also increased ZO-1 expression, decreased CDH1 expression and regulated the TLR4/NF-κB signalling pathway.

Platelet-rich plasma treatment may improve the expression of ZO-1 and CDH1 in urinary epithelium in vitro by mediating the TLR4/NF-κB pathway, which is effective in the treatment of IC.