Hydroxycitric acid inhibits ferroptosis and ameliorates benign prostatic hyperplasia by upregulating the Nrf2/GPX4 pathway
Abstract
Benign prostatic hyperplasia (BPH) poses a significant public health challenge, affecting a substantial portion of aging men worldwide. Current therapeutic options offer limited efficacy. The pathogenesis of BPH is multifactorial, involving ferroptosis, oxidative stress, and chronic inflammation. Hydroxycitric acid (HCA) is a natural compound with diverse pharmacological activities, including the inhibition of ferroptosis, anti-inflammatory, anti-oxidative stress, and anti-tumor effects. However, its role in BPH remains unexplored. This study aimed to investigate the effects of HCA on BPH and elucidate the underlying mechanisms, with the goal of providing novel therapeutic insights for BPH treatment. C57BL/6J mice were used to establish a BPH model induced by testosterone propionate (TP). Animals were then randomly assigned to the following groups: Sham, BPH, BPH + Lip-1, BPH + Bru, BPH + HCA + Bru, and BPH + HCA. Prostate index (PI) was determined, and histopathological changes were evaluated by hematoxylin and eosin (HE) staining. Mitochondrial morphology was analyzed by TEM. The levels of Fe2+, MDA, and GSH in prostate tissues were measured. Western blot analysis was performed to assess the protein expression of Nrf2 and GPX4.Results: Compared to the Sham group, the prostate tissues of the BPH group exhibited typical histopathological features of hyperplasia, including epithelial cell proliferation, increased glandular lumen size. Concurrently, the levels of ferroptosis…
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Evidence Hub reads this as a randomized trial. Its evidence level is 2 of 5 (High · randomized trial). Randomized trials of a reasonable size are the strongest single-study design.
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