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Background <p>Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a prevalent urological condition marked by ongoing pelvic pain, inflammation, and a reduced quality of life. Increasing evidence indicates that dysregulated immune responses and oxidative stress contribute to CP/CPPS pathogenesis. Myricetin (MYR), a natural flavonoid, has been reported to exert anti-inflammatory and antioxidant effects in multiple disease models. However, its role in CP/CPPS remains unclear.</p> Methods <p>The protective effects of MYR were evaluated in an experimental autoimmune prostatitis (EAP) mouse model and in lipopolysaccharide (LPS)-induced RWPE-1 prostate epithelial cells. Prostatic histopathology, pelvic pain behavior, inflammatory cytokine levels, immune cell infiltration, and oxidative stress markers were assessed in vivo. In vitro, inflammatory mediator expression, reactive oxygen species (ROS) production, oxidative stress status, mitochondrial function, and signaling pathway activation were examined using qRT-PCR, Western blotting, immunofluorescence, and biochemical assays. Network pharmacology analysis was used to predict potential targets and pathways associated with the effects of MYR. The involvement of Nrf2 signaling was further examined using the Nrf2 inhibitor ML385.</p> Results <p>MYR markedly alleviated prostatic inflammation and pelvic pain in EAP mice, accompanied by reduced serum levels of pro-inflammatory cytokines and chemokines, decreased infiltration of CD4-positive T cells and CD68-positive macrophages, and improved oxidative stress status. In LPS-induced RWPE-1 cells, MYR suppressed the expression of inflammatory mediators, reduced ROS accumulation, restored redox balance, and attenuated mitochondrial dysfunction. Mechanistically, MYR inhibited the phosphorylation of ERK, JNK, p38, and STAT3, suppressed NF-κB activation, and promoted Nrf2 signaling. Pharmacological inhibition of Nrf2 largely abolished the anti-inflammatory and antioxidant effects of MYR.</p> Conclusions <p>MYR attenuated inflammation, oxidative stress, and pain-related changes in experimental prostatitis, and these effects were associated with coordinated modulation of MAPK, STAT3, NF-κB, and Nrf2 signaling pathways. These findings suggest that MYR may represent a potential candidate for further preclinical investigation in CP/CPPS.</p>

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Myricetin attenuates experimental autoimmune prostatitis and inflammatory and oxidative injury in LPS-induced RWPE-1 cells potentially through modulation of MAPK/STAT3/NF-κB/Nrf2 signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月23日

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  • Hang Zhang,
  • Dahong Zhang,
  • Yanping Zhang,
  • Zhenwei Han,
  • Zhihai Teng,
  • Yaxuan Wang

摘要

Background

Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a prevalent urological condition marked by ongoing pelvic pain, inflammation, and a reduced quality of life. Increasing evidence indicates that dysregulated immune responses and oxidative stress contribute to CP/CPPS pathogenesis. Myricetin (MYR), a natural flavonoid, has been reported to exert anti-inflammatory and antioxidant effects in multiple disease models. However, its role in CP/CPPS remains unclear.

Methods

The protective effects of MYR were evaluated in an experimental autoimmune prostatitis (EAP) mouse model and in lipopolysaccharide (LPS)-induced RWPE-1 prostate epithelial cells. Prostatic histopathology, pelvic pain behavior, inflammatory cytokine levels, immune cell infiltration, and oxidative stress markers were assessed in vivo. In vitro, inflammatory mediator expression, reactive oxygen species (ROS) production, oxidative stress status, mitochondrial function, and signaling pathway activation were examined using qRT-PCR, Western blotting, immunofluorescence, and biochemical assays. Network pharmacology analysis was used to predict potential targets and pathways associated with the effects of MYR. The involvement of Nrf2 signaling was further examined using the Nrf2 inhibitor ML385.

Results

MYR markedly alleviated prostatic inflammation and pelvic pain in EAP mice, accompanied by reduced serum levels of pro-inflammatory cytokines and chemokines, decreased infiltration of CD4-positive T cells and CD68-positive macrophages, and improved oxidative stress status. In LPS-induced RWPE-1 cells, MYR suppressed the expression of inflammatory mediators, reduced ROS accumulation, restored redox balance, and attenuated mitochondrial dysfunction. Mechanistically, MYR inhibited the phosphorylation of ERK, JNK, p38, and STAT3, suppressed NF-κB activation, and promoted Nrf2 signaling. Pharmacological inhibition of Nrf2 largely abolished the anti-inflammatory and antioxidant effects of MYR.

Conclusions

MYR attenuated inflammation, oxidative stress, and pain-related changes in experimental prostatitis, and these effects were associated with coordinated modulation of MAPK, STAT3, NF-κB, and Nrf2 signaling pathways. These findings suggest that MYR may represent a potential candidate for further preclinical investigation in CP/CPPS.