Protective Role of Agomelatine via Modulation of TLR4/NF-κB: NLRP3/IL-1β Signaling Pathways in Testosterone-Induced Benign Prostatic Hyperplasia in Rats

    Asmaa Mohamed Abdel‐Aziz, Sara M. Ahmed, Walaa Yehia Abdelzaher, Nada Amgad Mohamed, Alyaa E. Abdelkader, Rasha F. Ahmed, Asmaa Ali, Ahmed Kotb, Alyaa Abdelfattah Abdelmonaem
    TLDR Agomelatine may help reduce benign prostatic hyperplasia by blocking certain inflammatory pathways.
    This study investigated the effects of agomelatine (AGO) on testosterone-induced benign prostatic hyperplasia (BPH) in rats. Male rats treated with testosterone propionate to induce BPH showed improvements when pretreated with AGO, including reduced prostate index, serum PSA, and testosterone levels. Histological analysis indicated that AGO improved prostate tissue architecture and reduced oxidative stress, as evidenced by decreased lipid peroxidation and preserved glutathione levels. AGO also lowered pro-inflammatory cytokines, such as TLR4 and IL-1β, and decreased NLRP3 inflammasome and VEGF-A protein expressions. Additionally, AGO reduced the expression of NF-κB and MyD88 proteins. These findings suggest that AGO may alleviate BPH through the inhibition of TLR4/NFκB and NLRP3/IL-1β signaling pathways, indicating its potential as a therapeutic option for BPH management.
    Discuss this study in the Community →

    Research cited in this study

    4 / 4 results

    Related Community Posts Join

    1 / 1 results

    Similar Research

    5 / 19 results