维生素C具有针对动物胆固醇肝损伤的肝保护作用

Su Jong Yu

Prevention and restoration of hepatic fibrosis from chronic liver injury is essential for the treatment of patients with chronic liver diseases.已知维生素C具有肝保护作用，但其潜在机制尚不清楚，尤其是与肝纤维化相关的机制。在这里，我们分析了维生素C对胆汁酸诱导的肝细胞凋亡在体外和岩性胆酸（LCA）诱导的肝损伤中的影响（ - ）小鼠，不能与人类类似地合成维生素C。当用胆汁酸处理HuH-Bat细胞时，内质网应激相关JNK激活诱导凋亡，但维生素C减弱了胆汁酸诱导的体外肝细胞凋亡。 In our in vivo experiments, LCA feeding increased plasma marker of cholestasis and resulted in more extensive liver damage and hepatic fibrosis by more prominent apoptotic cell death and recruiting more intrahepatic inflammatory CD11b(+) cells in the liver of vitamin C-insufficient Gulo(-/-) mice compared to wild type mice which have minimal hepatic fibrosis.然而，当维生素C补充为维生素C的gulo（ - / - ）小鼠时，肝纤维化在野生型小鼠中的维生素C含量（ - / - ）小鼠的肝脏中显着减弱，野生型小鼠和这种肝素c的这种肝癌的抗衰老症状都与抗衰老抗体相关。这些结果表明维生素C有他抗胆固性肝损伤的敏保护作用。