ArticleMolecular biology reports2026
2,8-Dihydroxyquinoline ameliorates oligoasthenozoospermia by inhibiting MAPK14-mediated spermatogonial ferroptosis.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundOligoasthenozoospermia (OAS) is a major cause of male infertility. 2,8-Dihydroxyquinoline (2,8-DHQ), an endogenous antioxidant metabolite, remains unexplored in OAS. This study identified 2,8-DHQ as a bioactive XHBG metabolite and elucidated its mechanisms in improving OAS. METHODS AND
resultsMale BALB/c mice received glycosides of Tripterygium wilfordii (GTW) (140 mg/kg/day, oral gavage) for 4 weeks to induce OAS, confirmed by marked reductions in testicular/epididymal weights, sperm concentration, serum testosterone, and severe seminiferous tubule disruption. Then, mice were treated with XHBG (10.4, 20.8, 41.6 g/kg/day) or 2,8-DHQ (50 mg/kg/day) for another 4 weeks. Integrative network pharmacology and serum metabolomics identified 2,8-DHQ as a key bioactive metabolite of XHBG, with 137 overlapping targets with OAS. In H
conclusion2,8-DHQ, an active metabolite of XHBG, ameliorates OAS by targeting MAPK14 to inhibit spermatogonial ferroptosis. These findings provide a scientific basis for the clinical use of XHBG and highlight 2,8-DHQ as a potential lead compound for male infertility.
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