Background Mitochondrial dysfunction in immature oocytes remains a critical barrier to successful in vitro maturation (IVM), particularly in cases of diminished ovarian reserve. While NAD + precursors are extensively studied, the direct impact of NADH - the reduced form central to electron transport - on human oocyte maturation remains unexplored. Methods Discarded GV/MⅠ oocytes from controlled ovarian hyperstimulation (COH) cycles were randomized to IVM media supplemented with NADH (10 -8 -10 –4 M). The optimal concentration (10 –6 M) was determined by embryonic development. Mechanistic analyses included: mitochondrial phenotyping, single-cell RNA sequencing (scRNA-seq) and intervention experiments. Results NADH boosted maturation rates by 26.31% and blastocyst rates by 23.4% versus controls. Mitochondrial indices surged (ATP, mitochondrial membrane potential, glutathione, all P 0.05), accompanied by ROS reduction. scRNA-seq and immunofluorescence results revealed NADH upregulated CDK2 and GAS6 genes. CDK2 inhibition suppressed maturation (5.13%), while NADH co-treatment partially restored rates (34.21%) after 24 hours. Exogenous GAS6 enhanced blastocyst formation by 44.44%. Conclusion This pilot study demonstrates that NADH, as a mitochondrial bioenergetic enhancer, ameliorates Human oocytes maturation and subsequent embryonic development, with this promotive effect appearing to be associated with upregulation of CDK2 and GAS6.
Zhang et al. (Wed,) studied this question.
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