生殖氧化应激损伤是导致男性不育的主要内因之一。课题组前期发现近江牡蛎多糖（ORP）能够缓解小鼠生殖氧化应激损伤，但其机制仍不明确。据报道，小鼠睾丸支持细胞（TM4）的自噬作用可拮抗氧化应激导致的凋亡，提高其存活率。课题组前期研究表明ORP能够调控TM4细胞中自噬关键蛋白p62的表达，因此推测“ORP可能通过调节TM4细胞自噬干预小鼠生殖氧化应激损伤”。为验证该假说，通过体内及体外模型，采用透射电子显微镜观察ORP对TM4细胞中自噬体水平的影响；采用DCFH-DA荧光探针、ELISA试剂盒分析ORP对细胞内ROS水平及抗氧化酶的影响；并利用qRT-PCR、Western blot、免疫荧光等手段检测ORP对自噬关键蛋白（LC3-Ⅱ、beclin1、p62）及下游抗氧化通路的影响。从整体、细胞及分子水平探讨自噬在ORP改善生殖氧化应激损伤中的作用及干预机制，为生殖氧化应激损伤的防治提供新思路。

Reproductive oxidative stress damage has been identified as a major internal cause of male infertility. In previous experiments, Ostrea rivularis polysaccharide (ORP) could reduce reproductive oxidative stress damage. But its mechanism is still unclear. As reported, autophagy in Sertoli TM4 cells (TM4) could antagonize oxidative stress apoptosis to increase the survival rate of TM4. Previous studies showed that ORP could regulate the expression of p62, which is a key protein of TM4 in autophagy. Therefore, it is speculated that ORP may intervene in reproductive oxidative stress through regulating autophagy of TM4 cell. In order to verify the hypothesis, transmission electron microscope is used to observe the effect of ORP on the technical level of autophagosomes in TM4 in vivo and in vitro. The DCFH-DA fluorescence probe and ELISA kit are applied to analyze influence of ORP on the level of ROS in cells and antioxidant enzyme. Finally, qRT-PCR, Western blot and immunofluorescence are used to detect the effect of ORP on autophagy key proteins (LC3-II, beclin1, p62) and downstream antioxidant pathways. The mechanism of autophagy in reducing reproductive oxidative stress injury of ORP will be discussed in the whole, cell and molecular level, which will provide new ideas for the prevention and treatment of reproductive oxidative stress injury.