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ZHU Liang-liang, WU Xue-yin, LIU Xin.et al, . Protective effect of 2,4-dihydroxybenzophenone on DMN induced acute hepatotoxicity in mice[J]. Chinese Journal of Public Health, 2014, 30(2): 206-208. DOI: 10.11847/zgggws2014-30-02-24
Citation: ZHU Liang-liang, WU Xue-yin, LIU Xin.et al, . Protective effect of 2,4-dihydroxybenzophenone on DMN induced acute hepatotoxicity in mice[J]. Chinese Journal of Public Health, 2014, 30(2): 206-208. DOI: 10.11847/zgggws2014-30-02-24

Protective effect of 2,4-dihydroxybenzophenone on DMN induced acute hepatotoxicity in mice

  • ObjectiveTo investigate the protective effect of 2,4-dihydroxybenzophenone (BP-1) on acute hepatotoxicity induced by dimethylnitrosamine(DMN) in mice.MethodsTwenty-five male ICR mice with body weight of 18-22 g were divided into control group,model group,low,moderate,and high dose BP-1 exposure group (200,400,and 800 mg/kg).BP-1 was administrated to the mice in exposure groups for 4 days and DMN was injected into the mice 30 min after BP-1 administration on the 4th day.Twenty-four hours after the treatment,all mice were killed and activities of serum alanine aminotransferase (ALT),aspartate aminotransferase (AST),and lactate dehydrogenase (LDH) were measured.The contents of reduced glutathione (GSH),oxidized glutathione (GSSG),and malonaldehyde (MDA) were also determined.Histopathological changes of liver were observed.ResultsSerum ALT,AST and LDH activities of DMN group were significantly increased compared with those of the vehicle control group (P<0.01 for all).The content of MDA was increased to 0.256±0.059 μmol/g (P<0.01).Histopathological observations revealed a severe injury of liver.Serum ALT,AST and LDH activities of BP-1 group were significantly decreased compared with those of the model group (P<0.05 for all).The ratio of GSH/GSSG was increased and the content of MDA was decreased(0.062±0.034 μmol/g,P<0.01).Histopathological observations also revealed an ameliorated change of liver.ConclusionThe results indicate that 2,4-dihydroxybenzophenone has protective effect on acute hepatotoxicity induced by DMN in mice.
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