Lycopene attenuates chronic prostatitis/chronic pelvic pain syndrome by inhibiting oxidative stress and inflammation via the interaction of NF-κB, MAPKs, and Nrf2 signaling pathways in rats

番茄红素通过 NF-κB、MAPK 和 Nrf2 信号通路的相互作用抑制氧化应激和炎症,从而减轻大鼠慢性前列腺炎/慢性盆腔痛综合征

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作者:Qinxin Zhao, Feiya Yang, Lingquan Meng, Dong Chen, Mingshuai Wang, Xinxing Lu, Dexi Chen, Yongguang Jiang, Nianzeng Xing

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.

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.

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.

Objective

This study aimed to observe the effect of lycopene on CP/CPPS and to explore the underlying mechanisms. Materials and

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.

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