酒精性肝损伤, 肝阴虚证, 环磷酸腺苷, 环磷酸鸟苷, 动物模型

Objective Based on the mouse model of chronic alcoholic liver injury induced by Lieber DeCarli liquid alcohol feed, intragastric administration of thyroxine to mice to make a model of liver yin deficiency syndrome of alcoholic liver injury. The model was explored from two aspects: thyroxine concentration and experimental cycle. Methods ICR mice were randomly divided into blank group,PTH 0. 16 g / kg +15 d group, PTH 0. 32 g / kg +15 d group, PTH 0. 64 g / kg +15 d group, PTH 0. 16 g /kg +30 d group, PTH 0. 32 g / kg +30 d group, and PTH 0. 64 g / kg +30 d group, with 10 mice in each group. The mouse model of liver yin deficiency syndrome of alcoholic liver injury was prepared by gavage with Lieber-DeCarli alcohol liquid feed and different concentrations of thyroid hormone in different cycles. After 15 or 30 days, the state of mice in each group was observed, body weight, body temperature, heart rate were measured, serum transaminase activity, cyclic nuclear adenosine, liver lipid, antioxidant enzyme activity and cytokine levels in liver tissue were measured, and the liver was  taken for HE pathological examination. Results Compared with the blank group, the mice in PTH 0. 32 g / kg +30 d group had significantly reduced body weight, increased body temperature, accelerated heart rate, dull hair, fatigue, irritability, dry stool, yellow urine and other symptoms(P<0. 05) . The levels of serum ALT, AST, cAMP and MDA、TC、TG、IL-6 in liver tissue increased significantly ( P< 0. 01, P< 0. 05) . The levels of cGMP in serum and SOD、IL-10 in liver tissue decreased significantly ( P<0. 01,P< 0. 05 ) . Lipid deposition and hepatocyte necrosis occurred in the liver. Conclusion Successfully established a mouse model of alcoholic liver injury with liver yin deficiency syndrome.

alcoholic liver injury, liver yin deficiency syndrome, cAMP, cGMP, animal model