酒精性肝损伤是危害我国饮酒人群健康的重要疾病。研究表明，酒精性肝损伤患者体内往往存在硒缺乏。硒是一种具有抗氧化功能的必需微量元素。一定剂量的硒在发挥抗氧化作用的同时，还具有激活胰岛素信号作用。我们的前期研究证实激活胰岛素信号可以调控Redox稳态和ADH1-ALDH2平衡进而减轻酒精性肝损伤，提示补硒也可能通过增强胰岛素信号对酒精性肝损伤发挥保护作用。但硒的生理需求浓度和中毒浓度之间的安全区较窄，过度补硒具有显著副作用，筛选针对酒精性肝损伤的合理补硒剂量至关重要。鉴于拮抗酒精性肝损伤的合理补硒剂量及机制目前尚不清楚，本课题将从细胞-动物两个层面，综合利用生化检测和分子生物学技术手段，结合酒精性肝损伤的发病机制及硒的作用特点，探索拮抗酒精性肝损伤的合理补硒剂量并揭示其效应通路和分子机制。本课题将为以适度补硒为策略的酒精性肝损伤防治措施提供理论和实验依据。

Alcoholic liver injury is an important disease that harms the health of drinking people in China. Studies have shown that selenium deficiency is often present in patients with alcoholic liver injury. Selenium is an essential trace element with antioxidant function. A certain dose of selenium has an antioxidant effect and also activates insulin signaling. Our previous studies have demonstrated that activation of insulin signaling can regulate Redox homeostasis and ADH1-ALDH2 balance to reduce alcoholic liver damage, suggesting that selenium supplementation may also protect alcohol-induced liver injury by enhancing insulin signaling. However, the safe area between selenium physiological demand concentration and poisoning concentration is narrow, and excessive selenium supplementation has significant side effects. It is important to screen a reasonable dose of selenium for alcoholic liver injury. In view of the reasonable dose and mechanism of selenium supplementation against alcoholic liver injury, it is still unclear. This topic will combine the biochemical detection and molecular biology techniques from the cell-animal level, combined with the pathogenesis of alcoholic liver injury and selenium. The characteristics of the role, explore the rational dose of selenium to antagonize alcoholic liver injury and reveal its effector pathway and molecular mechanism. This topic will provide theoretical and experimental basis for the prevention and treatment of alcoholic liver injury with moderate selenium as a strategy.