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Background: Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is identified as a urinary andrological diseases that afflict men due to various discomforts. It is urgent and meaningful to develop the novel and effective treatments as a result of the unclear etiology and dismal therapeutic effect of CP/CPPS. Lycopene exerts a crucial role in numerous chronic inflammatory diseases owing to its potent antioxidant capacity. Objective: This study aimed to observe the effect of lycopene on CP/CPPS and to explore the underlying mechanisms. Materials and Methods: A CP/CPPS model with complete Freund's adjuvant was established in this study. Afterward, intragastric lycopene or corn oil was administered daily for 4 consecutive weeks. Finally, the cardiac blood and prostate tissue samples were collected from rats to carry out related evaluation and testing. Results: It was found in this study that lycopene alleviated changes in prostate histopathology compared with those in the complete Freund's adjuvant‐induced CP/CPPS model rats without lycopene treatment. Furthermore, lycopene was suggested to reduce the levels of chemokines MCP1 and MIP‐1α, down‐regulate the expression levels of cytokines (such as TNFα, IL‐1β, IL‐2, and IL‐6), and up‐regulate those of CAT, GSH‐PX, and T‐SOD, decrease that of malondialdehyde. Moreover, it also inhibited the phosphorylation of MAPKs, NF‐κB, and enhanced phosphorylation of the Nrf2 in the CP/CPPS rat model. Discussion and Conclusions: The findings in this study suggest that lycopene exerts potent anti‐ CP/CPPS Seffects through alleviating inflammatory response and oxidative stress, which is probably attributed to the interaction of NF‐κB, MAPKs, and Nrf2 signaling pathways in rats. As a natural antioxidant, lycopene may serve as a promising pharmaceutical preparation for treating CP/CPPS. [ABSTRACT FROM AUTHOR]

Chronic prostatitis is a common urological disease. The etiology of this disease and effective therapy for its treatment are yet to be elucidated. We investigated the functions of XLQ® in chronic nonbacterial prostatitis using a complete Freund's adjuvant‐induced rat model. Prostates and blood samples were collected for further evaluation after oral gavage with XLQ ® or a vehicle for 4 weeks. The results showed that XLQ ® significantly decreased the prostate index, ameliorated the histopathologic changes, and reduced CD3+ and CD45+ cell infiltration in the prostate stroma. Further study showed that XLQ ® suppressed the expression of proinflammatory cytokines, such as interleukin (IL)‐1β, IL‐2, IL‐6, IL‐17A, monocyte chemoattractant protein‐1, and tumor necrosis factor‐α. XLQ ® showed a strong antioxidant capacity by enhancing the activities of antioxidative enzymes (e.g., total superoxide dismutase, catalase, and glutathione peroxidase) and decreasing the level of lipid peroxidation products (malondialdehyde). Moreover, XLQ ® can suppress the activation of nuclear factor‐κB and P38‐mitogen‐activated protein kinase signaling pathways. In summary, XLQ ® has affirmative effects on chronic prostatitis, which could be attributed to its anti‐inflammatory and antioxidative capacities. On the basis of these results, XLQ ® can be developed as an effective and safe therapy for chronic prostatitis. [ABSTRACT FROM AUTHOR]