目的探讨草苁蓉多糖对过氧化氢(H_2O_2)致张氏肝细胞氧化损伤的保护作用及机制。方法以张氏肝细胞为研究对象,用H_2O_2诱导建立细胞氧化应激损伤模型,噻唑蓝法检测细胞存活率;分光光度法测定细胞外液中谷丙转氨酶(ALT)、谷草转氨酶(AST)、乳酸脱氢酶(LDH)及细胞中丙二醛(MDA)、还原型谷胱甘肽(GSH)和超氧化物歧化酶(SOD)含量。结果与对照组比较,模型组肝细胞存活率[(52.5±1.2)%]下降,细胞外液中ALT、AST、LDH活力[分别为(23.5±2.9)、(29.4±2.9)、(595.4±5.6)U/L]升高,细胞中SOD活性和GSH含量[分别为(163.1±6.1)U/mg prot、(8.91±1.26)mg/g prot]下降,丙二醛含量[(12.6±2.6)nmol/mg prot]升高;与模型组比较,50 mg/L草苁蓉多糖组肝细胞存活率[(79.0±5.5)%]升高,细胞外液中ALT、AST、LDH活力[分别为(10.4±2.9)、(14.4±3.2)、(374.4±12.5)U/L]降低,细胞中SOD活性和GSH含量[分别为(323.6±17.3)U/mg prot、(15.4±0.52)mg/g prot]升高,细胞MDA含量[(6.93±0.75)nmol/mg prot]降低。结论草苁蓉多糖对H_2O_2所致张氏肝细胞损伤具有一定保护作用,其机制可能与提高细胞抗氧化能力有关。 Objective To investigate the protective effects and mechanisms of cistanche desertica on oxidative damage of Hepatic hepatocytes induced by hydrogen peroxide (H 2 O 2). Methods Zhang’s hepatocytes were used as experimental subjects. H 2 O 2 -induced model of cell oxidative stress injury was established. Cell viability was measured by thiazolyl blue assay. The levels of ALT, AST, Dehydrogenase (LDH) and malondialdehyde (MDA), reduced glutathione (GSH) and superoxide dismutase (SOD) in the cells. Results Compared with the control group, the survival rate of hepatocytes in model group decreased (52.5 ± 1.2%), the activities of ALT, AST and LDH in the extracellular fluid were (23.5 ± 2.9), (29.4 ± 2.9) and (595.4 ± (P <0.01). The activity of SOD and the content of GSH in the cells [(163.1 ± 6.1) U / mg prot and (8.91 ± 1.26) mg / ) nmol / mg prot]. Compared with the model group, the survival rate of hepatocytes in [(79.0 ± 5.5)%] of 50 mg / L Cistanche desertica polysaccharide group increased and the activities of ALT, AST and LDH in extracellular fluid (323 ± 17.3) U / mg prot and (15.4 ± 0.52) mg respectively, which were (10.4 ± 2.9), (14.4 ± 3.2) and (374.4 ± 12.5) U / / g prot] increased, MDA content [(6.93 ± 0.75) nmol / mg prot] decreased. Conclusion Polysaccharide of Cistanche deserticola has some protective effects on H 2 O 2 -induced Zhang’s hepatocyte injury. The mechanism may be related to the enhancement of cell antioxidant capacity.