Treatment of Premature Ovarian Failure Based on “Mitochondrial-Oxidative Stress” Damage Mechanism from the “Stasis” Theory

卵巢早衰(premature ovarian failure, POF)的患病率在近年逐步攀升，其发病机制尚不明确。过量的活性氧引起线粒体损伤，造成氧化应激，因此“线粒体–氧化应激”损伤机制是POF的关键机制。此文通过梳理和总结国内外“线粒体–氧化应激”损伤机制的研究和报道，将氧化应激损伤和POF的关键病理因素“血瘀”结合，从而建立POF“血瘀–氧化应激–炎症”的中西医结合病理理论，在此基础上深入探讨POF的修复机制和潜在的治疗靶点，论述“治瘀法”的有效性和科学性，为中医药防治POF提供新的思路。The prevalence of premature ovarian failure (POF) has been increasing in recent years, and the pathogenesis of POF is still unclear. Excessive reactive oxygen species (ROS) cause mitochondrial damage and oxidative stress, and thus the “mitochondrial-oxidative stress” damage mechanism is a key mechanism of POF. In this paper, we review and summarize the studies and reports on the damage mechanism of “mitochondrial-oxidative stress” at home and abroad, and combine oxidative stress injury with blood stasis, which is a key pathological factor of POF, to establish the “blood stasis-oxidative stress-inflammation” pathology theory of POF that combines traditional Chinese and Western medicines. Based on this, we deeply explore the repair mechanism and potential therapeutic targets of POF and discuss the effectiveness and scientific validity of the “treatment of blood stasis method”, to provide new ideas for the prevention and treatment of POF by TCM.