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目的探讨姜黄素对砷中毒小鼠急性肝脏毒性与氧化损伤的拮抗作用。方法选取60只健康的昆明种雌性小鼠,将60只小鼠分为对照组、单纯染毒组、干预组1和干预组2。对照组6只,单纯染毒组、干预组1和干预组2各18只。各实验组小鼠以自由饮水方式饮用浓度为10mg/L、50mg/L、100mg/L的含砷水,时间6周。干预组1、2分别给予姜黄素以200mg/kg、600mg/kg剂量进行灌胃干预,每周2次。对各实验组小鼠肝脏丙二醛含量、血清谷草转氨酶及谷丙转氨酶水平、肝脏和全血谷胱甘肽含量进行测定。结果单纯染毒组血清谷草转氨酶和谷丙转氨酶水平高于对照组,差异具有统计学意义(P<0.05)。单纯染毒组各水砷浓度条件下肝脏丙二醛含量均高于对照组,差异具有统计学意义(P<0.05)。水砷浓度相同的条件下,与单纯染毒组比较,干预组1及干预组2谷丙转氨酶和谷草转氨酶水明显降低,肝脏丙二醛含量下降,全血和肝脏谷胱甘肽含量上升,差异均具有统计学意义(P<0.05)。结论姜黄素对砷中毒小鼠急性肝脏毒性与氧化损伤具有一定的拮抗作用。
Objective To investigate the antagonistic effect of curcumin on acute liver toxicity and oxidative damage in mice with arsenism. Methods Sixty healthy Kunming female mice were selected and 60 mice were divided into control group, simple exposure group, intervention group 1 and intervention group 2. The control group of 6, simple exposure group, intervention group 1 and intervention group 2 each 18. Each experimental group of mice drinking water with free drinking concentration of 10mg / L, 50mg / L, 100mg / L of arsenic-containing water for 6 weeks. Intervention group 1 and 2 were given curcumin 200mg / kg, 600mg / kg dose for gavage intervention twice a week. The malondialdehyde (MDA), aspartate aminotransferase (AST) and alanine aminotransferase (AST), glutathione content in liver and whole blood of the mice in each experimental group were determined. Results Compared with the control group, serum aspartate aminotransferase (AST) and glutamic pyruvic transaminase (ALT) were higher in the control group (P <0.05). The content of malondialdehyde in the liver of arsenite-treated rats was significantly higher than that of the control group (P <0.05). Water arsenic concentration of the same conditions, compared with the simple exposure group, intervention group 1 and intervention group 2 alanine aminotransferase and aspartate aminotransferase water was significantly reduced liver malondialdehyde content decreased, whole blood and liver glutathione content increased, The differences were statistically significant (P <0.05). Conclusion Curcumin has antagonistic effect on acute liver toxicity and oxidative damage in mice with arsenism.