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.

中文翻译：

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绿原酸可减轻环磷酰胺诱导的大鼠间质性膀胱炎。

目的

本研究旨在探讨绿原酸（CGA）对环磷酰胺（CYP）诱导的大鼠间质性膀胱炎（IC）的治疗作用和分子机制。

材料和方法

通过在雌性Sprague-Dawley大鼠中腹膜内注射CYP建立IC的动物模型。将80只大鼠随机分为四组：阴性对照组（NC），CGA治疗的NC（NC + CGA），IC和CGA治疗的IC（IC + CGA）。通过分析尿动力学参数评估膀胱排尿功能。使用蛋白质印迹和免疫组织化学分析检测膀胱标本中凋亡相关蛋白和炎性生物标志物的表达。

主要发现

与IC组相比，IC + CGA组的膀胱泌尿功能明显改善。CGA治疗可减轻IC大鼠膀胱组织的炎症损伤。与IC + CGA组相比，IC组中Caspase3和Bax表达较高，而Bcl-2表达较低。另外，膀胱组织中炎症生物标志物的表达水平在两组之间存在显着差异。此外，CGA可以抑制CYP诱导的大鼠膀胱组织中MAPK /NF-κB磷酸化。

意义

在CYP诱导的IC大鼠模型中，CGA可减轻炎症和细胞凋亡，从而部分恢复膀胱功能，并且MAPK /NF-κB途径可能参与其中。