Scholarlink

Objective <p>To investigate the therapeutic effect of platelet-rich plasma (PRP) on a cyclophosphamide (CYP)-induced interstitial cystitis (IC) rat model.</p> Methods <p>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.</p> Results <p>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.</p> Conclusion <p>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.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

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

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年3月25日

查看全文
  • Yufan Wu,
  • Lei Chen,
  • Minzhe Xu,
  • Linya Yao,
  • Shiyao Yang,
  • Xiaojie Ang,
  • Weiguo Chen

摘要

Objective

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

Methods

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.

Results

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.

Conclusion

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.