前期研究证实，补肾活血中药益精方能够有效治疗少弱精子症，并能够降低精浆活性氧水平，提高精子线粒体膜电位，抑制精子早期凋亡。结合自噬与凋亡最新进展，提出假说1线粒体及其自噬这一特异性的清除途径，可能是调控生精微环境ROS 水平以及生精细胞发生凋亡、自噬之间平衡的纽带，假说2补肾活血中药可从抗氧化应激，保护线粒体功能稳定，调节自噬与凋亡平衡，改善生精微环境。以特发性少弱精症患者治疗前后精子标本、CP诱导的小鼠氧化应激不育模型、体外ACR诱导Leydig细胞损伤模型为对象，以ROS与线粒体功能为中心，探讨LC3、Beclin-1、PI3K/AKT/mTOR等自噬因子，与Caspase-3, Bcl-2和Bax等凋亡因子，对生精相关细胞自噬与凋亡的调控作用，深入阐释补肾活血方药治疗少弱精症的分子机制，为丰富中医药理论科学内涵、不断提高疗效服务。

Previous studies demonstrated that traditional Chinese medicine Yi Jing Fang can be effective in the treatment of oligoasthenozoospermia, and be able to reduce the level of reactive oxygen species in seminal plasma, improve sperm mitochondrial membrane potential, inhibition of early sperm apoptosis. Autophagy and apoptosis combined the latest developments, and put forward the hypothesis 1 mitochondrial autophagy this specific route of elimination, regulation may be subtle green environment ROS level and spermatogenic cell apoptosis, autophagy balance between self-ties, hypotheses 2 traditional Chinese medicine from oxidative stress, mitochondrial function protection and stability, regulating autophagy and apoptosis balance, improve student subtle environment. In front less weak azoospermia treatment of patients with idiopathic sperm samples, CP-induced oxidative stress in mice infertile model, Leydig cell damage induced in vitro ACR model object to ROS and mitochondrial function as the center and explore LC3, Beclin-1 , PI3K / AKT / mTOR autophagy and other factors, and Caspase-3, Bcl-2 and Bax apoptosis and other factors related to spermatogenic cell autophagy and apoptosis regulation, in-depth interpretation of the treatment of kidney and promoting blood circulation less weak azoospermia the molecular mechanism for the rich scientific connotation of Chinese medicine theory, and constantly improve the efficacy of service.