The aim of this study was to investigate the effects of pyrroloquinoline quinone (PQQ), an oxidoreductase cofactor, on the H₂O₂-induced premature senescence model in HEI-OC1 auditory cells and to elucidate its mechanism of action in vitro. Cells were treated with PQQ for 1 day before H₂O₂ (100 μM) exposure. Mitochondrial respiratory capacity was damaged in this premature senescence model but was restored in cells pretreated with PQQ (0.1 nM or 1.0 nM). A decrease in mitochondrial potential, the promotion of mitochondrial fusion and the accelerated movement of mitochondria were all observed in PQQ-pretreated cells. The protein expression of sirtuin 1 (SIRT1) and peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) were significantly decreased under H₂O₂ exposure while they were increased with PQQ pretreatment, and PGC-1α acetylation was significantly decreased. In conclusion, PQQ has a protective effect on the premature senescence model of HEI-OC1 auditory cells and is associated with the SIRT1/PGC-1α signaling pathway, mitochondrial structure, and mitochondrial respiratory capacity.

本研究旨在探讨氧化还原酶辅助因子吡咯并喹啉醌 (PQQ) 对 H ₂ O ₂诱导的 HEI-OC1 听觉细胞过早衰老模型的影响，并阐明其体外作用机制。_{在 H 2} O ₂之前用 PQQ 处理细胞 1 天(100 μM) 曝光。在这种过早衰老模型中，线粒体呼吸能力受损，但在用 PQQ（0.1 nM 或 1.0 nM）预处理的细胞中得以恢复。在 PQQ 预处理的细胞中均观察到线粒体电位降低、线粒体融合促进和线粒体运动加速。_{在 H 2} O ₂下，sirtuin 1 (SIRT1) 和过氧化物酶体增殖物激活受体 γ coactivator-1α (PGC-1α) 的蛋白表达显着降低PQQ 预处理增加了暴露量，而 PGC-1α 乙酰化显着降低。综上所述，PQQ 对 HEI-OC1 听觉细胞早衰模型具有保护作用，并与 SIRT1/PGC-1α 信号通路、线粒体结构和线粒体呼吸能力有关。