猪精子17 ºC液态保存中受精能力持续下降,严重阻碍了猪精液的高效利用。氧化应激是导致精子受精能力下降的重要因素。前期研究筛选出的精子载脂蛋白A1（APOA1）和钙粘蛋白1（CDH1）与精子耐受氧化应激密切相关，研究表明其通过LKB1的介导调节AMPK的活性影响细胞存活，但具体机制仍不清楚。本研究以17 ºC液态保存的猪精子为研究对象，采用体外精子热应激模型，利用流式细胞术、Western blot、免疫共沉淀和免疫共定位等技术，首先确定APOA1和CDH1表达水平和氧化应激以及精子AMPK活性的相关性；其次揭示APOA1和CDH1如何通过LKB1的介导激活AMPK，以及活化的AMPK调节猪精子耐受氧化应激的机制，最终阐明APOA1/CDH1-LKB1-AMPK通路对猪精子耐受氧化应激的调控机制。本研究将为研究猪精子受精能力受损的机制提供新思路，为高质量猪精液的生产提供理论依据。

During liquid storage at 17 ºC, continuous decline of boar sperm fertilization capacity greatly impedes the efficient use of boar semen. Oxidative stress is most responsible to that. Our previous studies showed that apolipoprotein A1 (APOA1) and cadherin type 1 (CDH1) are deeply involved in sperm resistance to oxidative stress, and evidences showed that LKB1 mediates those two proteins to activate AMPK, consequently influencing cell survival. However, the underlying mechanism needs to be elucidated. This project will investigate on liquid-stored boar semen at 17 ºC, adopting an in vitro oxidative stress-induced model, utilizing flow cytometry, Western blot, co-immunoprecipitation, co-localization and other techniques. Firstly, the correlationship among APOA1/CDH1, oxidative stress, and AMPK activity will be studied; Secondly, how LKB1 mediates APOA1/CDH1 to activate AMPK will be disclosed, consequently the mechanism of activated AMPK regulates sperm resistance to oxidative stress will be studied; Finally, the regulatory mechanism of APOA1/CDH1-LKB1-AMPK on sperm resistance to oxidative stress will be elucidated. This study will provide new insights in the research on the mechanism how oxidative stress provokes compromise of sperm fertilization capacity, and theoretical information on promoting high-quality boar semen production.