目的探讨橙皮苷对刀豆蛋白A(ConA)所致小鼠免疫性肝损伤的保护作用。方法小鼠随机分为正常组、模型组、联苯双酯组、橙皮苷低、中、高剂量组,各组分别灌胃给药7 d,采用尾静脉注射ConA建立急性肝损伤模型,检测各组小鼠肝脾指数,测定血清谷丙转氨酶(ALT)和谷草转氨酶(AST)水平,检测肝匀浆中谷胱甘肽(GSH)、丙二醛(MDA)含量和caspase-3活性和TNF-α水平,观察肝组织病理学变化。结果与正常组比较,模型组肝脾指数显著增高,肝组织炎性坏死明显,血清ALT、AST升高,肝匀浆中GSH含量显著降低,MDA含量显著升高,同时肝组织caspase-3活性和TNF-α水平亦显著增高(均P<0.01)。与模型组比较,橙皮苷能显著降低肝脾指数,改善肝组织损伤程度,降低血清ALT、AST水平,提高肝匀浆中GSH水平,降低MDA含量,降低caspase-3活性和TNF-α水平(P<0.05,P<0.01)。结论橙皮苷对ConA诱导的小鼠免疫性肝损伤具有一定的保护作用,其机制可能与抑制氧化应激反应,清除自由基,抑制TNF-α释放及caspase-3活化有关。 Objective To investigate the protective effect of hesperidin on immune hepatic injury induced by concanavalin A (ConA) in mice. Methods Mice were randomly divided into normal group, model group, bifendate group, hesperidin low, middle and high dose groups. Each group was administered intragastric administration for 7 days, and acute liver injury model was established by tail vein injection of ConA. The liver and spleen index of each group of mice was measured to determine the levels of serum glutamic-pyruvic transaminase (ALT) and aspartate aminotransferase (AST), and the levels of glutathione (GSH), malondialdehyde (MDA) and caspase-3 in liver homogenate were measured. TNF-α levels, observed histopathological changes in the liver. Results Compared with the normal group, the liver and spleen index of the model group increased significantly, the inflammatory necrosis of the liver tissue was obvious, serum ALT, AST increased, GSH content in liver homogenate decreased significantly, MDA content increased significantly, and liver caspase-3 activity was also observed. And TNF-α levels were also significantly increased (both P <0.01). Compared with the model group, hesperidin can significantly reduce the liver and spleen index, improve the degree of liver injury, reduce serum ALT, AST levels, increase the level of GSH in liver homogenate, reduce MDA content, reduce caspase-3 activity and TNF-α levels (P<0.05, P<0.01). Conclusion Hesperidin has protective effects on ConA-induced immune liver injury in mice. The mechanism may be related to the inhibition of oxidative stress, scavenging free radicals, inhibition of TNF-α release and caspase-3 activation.