1. Academic Validation
  2. Chlorogenic acid attenuates cyclophosphamide-induced rat interstitial cystitis

Chlorogenic acid attenuates cyclophosphamide-induced rat interstitial cystitis

  • Life Sci. 2020 Aug 1;254:117590. doi: 10.1016/j.lfs.2020.117590.
Jing Luo 1 Chengfei Yang 1 Xing Luo 1 Yang Yang 1 Jia Li 1 Bo Song 1 Jiang Zhao 1 Longkun Li 2
Affiliations

Affiliations

  • 1 Department of Urology, Second Affiliated Hospital, Army Military Medical University, Chongqing, People's Republic of China.
  • 2 Department of Urology, Second Affiliated Hospital, Army Military Medical University, Chongqing, People's Republic of China. Electronic address: lilongk@hotmail.com.
Abstract

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.

Keywords

Chlorogenic acid; Interstitial cystitis; MAPK/NF-κB.

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