评估姜黄素和/或维生素 C 在甲氨蝶呤引起的肝毒性中的保肝作用。实验研究在伊拉克巴格达穆斯坦西里亚大学医学院药理学系以及伊拉克癌症和医学遗传学研究中心进行，从2020年11月12日到2021年6月1日，由3-4个月大、每只体重30-40克的瑞士白化雌性小鼠组成。将小鼠分为5组并治疗10天。第1组接受蒸馏水，第2组在试验第10天接受单剂量甲氨蝶呤，第3组接受姜黄素加甲氨蝶呤治疗，第4组接受维生素C加甲氨蝶呤治疗，第5组接受姜黄素和维生素C治疗加甲氨蝶呤。测量的参数包括血清丙氨酸转氨酶、天冬氨酸转氨酶、碱性磷酸酶和乳酸脱氢酶，以及肝组织丙二醛、超氧化物歧化酶和谷胱甘肽。数据采用SPSS 16进行分析。小鼠35只； 5 组中每组 7 人（20%）。乳酸脱氢酶和丙二醛水平的降低反映了姜黄素产生的肝脏保护作用是显着的（p<0.05）。维生素 C 还具有显着的肝脏保护作用，通过降低丙氨酸转氨酶、碱性磷酸酶、乳酸脱氢酶和丙二醛水平即可证明。姜黄素和维生素 C 的组合反映了丙二醛显着降低所证明的累加效应 (p<0.05)。姜黄素和/或维生素 C 通过调节氧化应激生物标志物提供肝脏保护，防止甲氨蝶呤诱导的肝毒性。

To assess the hepatoprotective effect of curcumin and/or vitamin C in methotrexate-induced hepatotoxicity.The experimental study was conducted at the Department of Pharmacology, College of Medicine, and the Iraqi Centre for Cancer and Medical Genetic Research, Mustansiriya University, Baghdad, Iraq, from Nov 12, 2020, to June 1, 2021, and comprised Swiss albino female mice aged 3-4 months and weighing 30-40g each. The mice were divided into 5 groups and treated for 10 days. Group 1 received distilled water, group 2 received single-dose methotrexate on the 10th day of the trial, group 3 was treated with curcumin plus methotrexate, group 4 was treated with vitamin C plus methotrexate, and group 5 was treated with curcumin and vitamin C plus methotrexate. Parameters measured were serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and lactate dehydrogenase, as well as hepatic tissue malondialdehyde, superoxide dismutase and glutathione. Data was analysed using SPSS 16.There were 35 mice; 7(20%) in each of the 5 groups. Hepatoprotection produced by curcumin as reflected by a decrease in lactate dehydrogenase and malondialdehyde levels was significant (p<0.05). Vitamin C also produced a significant hepatoprotection, demonstrated by a decrease in alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase and malondialdehyde levels. The combination of curcumin and vitamin C reflected an additive effect demonstrated by a significant decrease in malondialdehyde (p<0.05).Curcumin and/or vitamin C provided hepatoprotection against methotrexate-induced hepatotoxicity through modulation of oxidative stress biomarkers.