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The effect of pirfenidone on rat chronic prostatitis/chronic pelvic pain syndrome and its mechanisms
Author(s) -
Peng Xufeng,
Guo Hailin,
Chen Jun,
Wang Jihong,
Huang Jianwen
Publication year - 2020
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.23995
Subject(s) - pirfenidone , medicine , prostatitis , chronic prostatitis/chronic pelvic pain syndrome , proinflammatory cytokine , oxidative stress , pharmacology , glutathione , inflammation , prostate , idiopathic pulmonary fibrosis , chemistry , biochemistry , cancer , lung , enzyme
Background Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is an intractable problem of the urogenital system. The aetiopathogenesis and effective treatments for CP/CPPS are needed to be untangled. Pirfenidone is a molecule that exhibits anti‐inflammatory, antifibrotic, and antioxidative stress capacities in a variety of animal experiments and clinical trials. This study was aimed to investigate the therapeutic effect of pirfenidone on CP/CPPS and to identify the mechanism responsible for it. Methods A CP/CPPS model was induced in rats by intraprostatic injection of complete Freund's adjuvant (CFA). Blood and prostatic tissues were harvested for assessment after the administration of pirfenidone or vehicle for 4 weeks. Results The findings revealed that pirfenidone significantly ameliorated chronic pelvic pain and inhibited prostatic inflammation and fibrosis. Further study found that pirfenidone suppressed the expression of proinflammatory mediators, including tumor necrosis factor‐α, interleukin‐1β (IL‐1β), IL‐6, IL‐8. Pirfenidone exhibited a potent antioxidant capacity through improving the activities of glutathione, catalase, total superoxide dismutase, and reducing the production of malondialdehyde. Furthermore, pirfenidone also facilitated the polarization of M2 macrophages and suppressed the activation of the nuclear factor‐κB (NF‐κB) signaling pathway. Conclusions Pirfenidone can exert a beneficial effect against CFA‐induced CP/CPPS by anti‐inflammatory, antioxidative, antifibrotic properties, and the function is mediated at least partly through the M2 polarization of macrophages and the inhibition of NF‐κB signaling pathway. These findings suggest that pirfenidone holds promise as a potential therapeutic for the treatment of CP/CPPS.