中文摘要：

观察虾青素（astaxanthin）对呼吸链复合体Ⅳ抑制剂叠氮钠（NaN3）损伤的人胎肝L-02细胞保护作用，并初步探讨其作用机制。100mmol·L^-1NaN3用于构建肝损伤细胞模型，通过测定不同浓度虾青素（0.01、0.10、1.00及1O.00nmol·L^-1）对损伤细胞存活率（MTT检测）、细胞内活性氧（reactive oxygen species，ROS）水平（DCFH-DA检测）、细胞凋亡率（Annexin V-FITC/PI双染法）以及线粒体膜电位（mitochondrial membrane potential，MMP）水平（JC-1法）的影响，发现虾青素能抑制损伤细胞晚期凋亡；对细胞存活率和MMP的保护作用呈现先增加后降低的非剂量依赖性关系，其中0.10nmol·L^-1虾青素表现为较强的保护作用；实验浓度范围内的虾青素并不能显著降低细胞内ROS水平（P〉0.05）。为进一步探讨虾青素对损伤细胞的保护作用，人工制备平面双层磷脂膜（planar bilayer lipidmembrane，BLM）模拟线粒体膜，测定不同浓度虾青素（0.1％、2.0％、10.0％）对H＋的传递能力。结果显示，虾青素对H＋传递效率无剂量依赖性，中等浓度（2.0％）的虾青素能够较高效率地传递H＋。结果提示，虾青素对NaN3损伤的人胎肝细胞的保护作用与其直接淬灭ROS的抗氧化功能无关，而可能是通过适当浓度下的虾青素对H＋的高效传递进而维持线粒体膜电位实现的。

英文摘要：

This study is to investigate the protective effect of astaxanthin against injured hepatocyte L-02 cells induced by sodium azide （NaN3） and reveal the possible mechanisms. Hepatocyte L-02 cells were exposed to 100 mmol·L^-1 NaN3 with various concentrations of astaxanthin pre-incubated, then the cell viability was measured by MTT method; The level of reactive oxygen species （ROS） was determined by DCFH-DA method; The changes of mitochondrial membrane potential （MMP） and apoptosis ratio were detected by JC-1 method and Annexin V-FITC/PI double stain method, respectively. Results showed that after cells were exposed to 100 mmol·L^-1 NaN3 for 3 hours, the cell viability significantly decreased; ROS level and the percentage of late phase apoptosis increased obviously; MMP was also declined. When cells were pretreated with astaxanthin, the cell damage and late phase apoptosis ratio reduced and MMP was maintained. However, the level of ROS showed insignificant decrease （P〉0.05）. The beneficial concentration of astaxanthin in improving cell viability and MMP was not in a dose dependent manner and the most effective of which was 0.10 nmol·L^-1 （P〈0.01）. Inorder to reveal its possible non-antioxidant mechanism, mitochondrial membrane was imitated and H＋ transferring function of astaxanthin was also detected by bilayer lipid membrane （BLM） method. Results showed that 2.0% astaxanthin could transfer H＋ efficiently. These suggested the mechanisms of astaxanthin in protection of hepatocyte L-02 cells not via its ROS quenching capability but via its H＋ transferring function, which improved the mitochondrial function and had the sequence biology effects.