Aims
This study aimed to investigate the therapeutic effect and molecular mechanism of chlorogenic acid (CGA) on cyclophosphamide (CYP)-induced rat interstitial cystitis (IC). Materials and
Methods
An animal model of IC was established by intraperitoneal injection of CYP in female Sprague-Dawley rats. Eighty rats were randomly assigned to four groups: negative control (NC), NC treated with CGA (NC + CGA), IC, and IC treated with CGA (IC + CGA). Bladder urination function was assessed by analyzing urodynamic parameters. The expression of apoptosis-related proteins and inflammatory biomarkers in bladder specimens was detected using western blot and immunohistochemistry analysis. Key findings: Compared with the IC group, bladder urinary function was significantly improved in the IC + CGA group. CGA treatment reduced inflammatory damage in the bladder tissue of IC rats. Caspase3 and Bax expression was higher while Bcl-2 expression was lower in the IC group compared to the IC + CGA group. In addition, there were significant differences between the groups in the expression levels of inflammatory biomarkers in the bladder tissue. Furthermore, CGA could inhibit CYP-induced MAPK/NF-κB phosphorylation in the rat bladder tissue. Significance: In a CYP-induced rat model of IC, CGA could reduce inflammation and apoptosis, thus partially restoring bladder function, and the MAPK/NF-κB pathway was probably involved in it.
Significance
In a CYP-induced rat model of IC, CGA could reduce inflammation and apoptosis, thus partially restoring bladder function, and the MAPK/NF-κB pathway was probably involved in it.