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

目的 在 Lieber-DeCarli 液体酒精饲料诱导的慢性酒精性肝损伤模型的基础上,灌胃甲状腺素制作酒精性肝损伤肝阴虚证小鼠模型,从甲状腺素浓度及实验周期两方面进行模型的探究。 方法将 ICR 小鼠随机分为空白组、甲状旁腺激素( PTH)0. 16 g / kg+15 d 组、PTH 0. 32 g / kg +15 d 组、PTH 0. 64 g / kg +15 d 组、PTH 0. 16 g / kg +30 d组、PTH 0. 32 g / kg +30 d 组、PTH 0. 64 g / kg +30 d 组,每组 10 只,用 Lieber-DeCarli 液体酒精饲料加不同浓度甲状腺素灌胃,不同周期制备小鼠酒精性肝损伤肝阴虚证模型。 15 或 30 d 后观察各组小鼠状态,测定体质量、体温、心率,检测血清转氨酶活性、环核腺苷酸水平及肝组织肝脂含量、抗氧化酶活性及细胞因子水平,并取肝进行苏木精-伊红染色( HE 染色)观察其病理组织学变化。 结果 与空白组相比,PTH 0. 32 g / kg +30 d 组小鼠体质量明显减轻,体温升高,心率加快,且出现毛发无光泽,疲倦易困,烦躁易怒,大便干小便黄等症状( P< 0. 05) 。 血清谷丙转氨酶(ALT) 、谷草转氨酶(AST) 、环磷酸腺苷( cAMP)水平及肝组织丙二醛( MDA) 、总胆固醇( TC) 、甘油三酯( TG) 、白细胞介素 6( IL-6)水平显著升高(P<0. 01,P< 0. 05) ;血清中环磷酸鸟苷( cGMP ) 水平及肝组织中超氧化物歧化酶( SOD) 、白细胞介素 10( IL-10)水平显著降低(P<0. 01,P<0. 05) ;肝出现脂质沉积及肝细胞坏死情况。 结论 成功构建酒精性肝损伤肝阴虚证小鼠模型。

酒精性肝损伤, 肝阴虚证, 环磷酸腺苷, 环磷酸鸟苷, 动物模型