Objective To research the role of phosphorylated signal transducer and activator of transcription 3 (p-STAT3) in the pathogenesis of alcoholic liver injury in mice.Methods Healthy and mature male mice were reared normally.They were divided at random into 5 groups,namely the normal group (n =10),the experimental-1 group (n =10),the experimental-2 group (n =10),the experimental-3 group(n =10),the experimental-4 group(n =10).The normal group was not treated.The mouse in experimental-1 group,experimental-2 group,experimental-3 group,experimental-4 group were given uninterruptedly 56 degree Beijing Red Star Erguotou by intragastric administration(14 mL · kg-1) for preparation of alcohol liver injury in mice.At the first week,the second week,the third week and the fourth week,respectively,the blood of mice was taken directly by eyeball enucleation.The serum levels of aspartate aminotransferase(AST) was measured with a aspartate aminotransferase assay kit.The expression levels of p-STAT3 in liver of mice was measured by Western blot.Results The serum levels of AST in normal group,experimental-1 group,experimental-2 group,experimental-3 group,experimental-4 group were (112 ±22),(126 ±24),(967 ±30),(1010 ±35),(206 ±23) U · L-1;comparison between experimental-1 group,experimental-4 group and normal group,the difference were without significantly (all P ＞ 0.05);comparison between experimemal-2 group,experimental-3 group and normal group,the difference had significantly (all P ＜ 0.01).The expression levels of p-STAT3 in the 5 groups were (0.52 ± 0.11),(3.21 ±0.33),(1.12 ± 0.21),(1.51 ± 0.23),(2.13 ± 0.26) AU;comparison between experimental-1 group,experimental-4 group and normal group,the difference had significantly (all P ＜ 0.01);comparison between experi mental-2 group,experimental-3 group and normal group,the difference had significantly(all P ＜0.05).ConclusionP-STAT3 may be involved in the acute phase response in the early stage of liver injury in mice,and participate in and promote hepatocyte injury.In the later stage,it may be beneficial to the regeneration,repair and inhibition of hepatocyte apoptosis.

Objective To investigate the dynamic changes and effects of tumor necrosis factor (TNF-α) expression in mice with alcohol-induced liver injury.Methods According to the principle of random distribution,50 mice were classified into two groups,including the normal control group(n =40) and the model group (n =10).Administered with alcohol of 56 degrees (15 mL · kg-1) for 1 week and 2,3,4 weeks to induce liver injury.All mice in control group were executed to obtain the eye blood and the liver tissue in 0 (control group),1 week and 2,3,4 weeks.The aspartate transaminase (AST) activities in mice were detected by Reitman-Frankel methods.With the detection of Western blotting,the expressions of TNF-α were measured in the mice of control group and model group in the process of alcohol-induced liver injury.Results The activity of AST in liver of mice at 0 (control group),1 week and 2,3,4 weeks were (112 ±22),(126 ±24),(967 ±30),(1010 ±35),(206 ±23) U · L-1,respectively.Compared with control group,the differences were significantly (all P ＜ 0.05).Compared with the control group,AST activities in the model group increased slowly in the first weeks,then rose rapidly in the second week,reached the peak in the third week,began to decline in the fourth week,but still higher than the control group.TNF-α level at 0,1 week and 2,3,4 weeks were 1.15 ±0.12,1.10±0.08,2.13 ±0.16,2.16 ±0.15,1.16 ±0.11 respectively.Compared with the control group,the differences were significantly(all P ＜0.01).Compared with the control group,the expression of TNF-α in the model group gradually rose from the first week to the third week,then fell close to normal level across time.Condusion The expression of TNF-α had obvious varieties in the process of alcoholic hepatic injury in mice,which demonstrates TNF-α may have significant impact on the injury and restoration of liver tissue.