Translational andrology and urology · 2026
Astaxanthin provides antioxidant protection in rats with chronic nonbacterial prostatitis by regulating the MAPK signaling pathway.
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Jiang Jiahao, Song Huajie, Chen Jing, Zeng Yan, Zhu Hengcheng, Ding Mao, Liu Lingqi
Аннотация
BACKGROUND: Chronic nonbacterial prostatitis (CNP) is the most common type of symptomatic prostatitis that afflicts men due to various discomforts. Owing to its anti-inflammatory and antioxidant properties, astaxanthin (AST) can be used in the treatment of various chronic inflammatory diseases. This study was conducted to assess the effects of AST and investigate the underlying mechanisms in a rat model of CNP.
METHODS: A rat model of CNP was established by intraprostatic carrageenan (0.1 mL 1% λ-carrageenan saline solution) injection. AST (40 and 80 mg/kg/day) was administered orally for 4 weeks, and blood and prostate tissue samples were collected for examination.
RESULTS: The prostate weight and index were lower in AST-treated rats than in rats with CNP. In prostate tissue and serum, AST increased superoxide dismutase and glutathione peroxidase activity. Meanwhile, AST reduced inflammatory factors [tumor necrosis factor-α, interleukin (IL)-1β, and IL-6] expression in prostate tissue and serum. Besides, AST also reduced nerve growth factor expression in prostate tissue. Furthermore, AST inhibited mitogen-activated protein kinase (MAPK) pathway activation.
CONCLUSIONS: This study showed that AST exerts antioxidant and protective effects against CNP, mediated through MAPK signaling suppression. The study results provide evidence supporting the potential use of AST in the treatment of CNP.
METHODS: A rat model of CNP was established by intraprostatic carrageenan (0.1 mL 1% λ-carrageenan saline solution) injection. AST (40 and 80 mg/kg/day) was administered orally for 4 weeks, and blood and prostate tissue samples were collected for examination.
RESULTS: The prostate weight and index were lower in AST-treated rats than in rats with CNP. In prostate tissue and serum, AST increased superoxide dismutase and glutathione peroxidase activity. Meanwhile, AST reduced inflammatory factors [tumor necrosis factor-α, interleukin (IL)-1β, and IL-6] expression in prostate tissue and serum. Besides, AST also reduced nerve growth factor expression in prostate tissue. Furthermore, AST inhibited mitogen-activated protein kinase (MAPK) pathway activation.
CONCLUSIONS: This study showed that AST exerts antioxidant and protective effects against CNP, mediated through MAPK signaling suppression. The study results provide evidence supporting the potential use of AST in the treatment of CNP.