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Updated: Jul 26, 2025

The Murine Choline-Deficient, Ethionine-Supplemented CDE Diet Model of Chronic Liver Injury
Published on: October 21, 2017
[Effects of curcumin on liver injury induced by chronic alcohol addiction]
Yi-Ming Wu1,2, Xue Lin3,4, Ya-Jing Su3,4
1College of Education, Ningxia University, Yinchuan 750021.
Abstract:
Objective: To investigate the intervention effects of curcumin (Curc) on liver injury induced by chronic alcohol addiction in mice. Methods: Thirty Balb/c mice were randomly divided into normal control group (Control), model group (Model), low-dose Curc group (5 mg/kg, Curc-L), medium dose Curc group (10 mg/kg, Curc-M) and high-dose Curc group (15 mg/kg, Curc-H), with 6 mice in each group. The chronic alcohol addiction liver injury model was prepared with 20% liquor. The mice in control group were given 2 ml of normal saline every day. The mice in model group were given 5 ml/kg of 20% liquor every day, and the mice in Curc treatment group were treated with Curc at the doses of 5, 10, 15 mg/kg in 2 ml saline every day for 35 days. The weight of liver was measured and the health status of mice was observed. Serum ALT, AST, ALP and liver TG, TC, HDL-C, LDL-C, MDA, SOD, GSH-Px and NO were measured. The pathological changes of liver tissues stained with hematoxylin and eosin were observed. Results: Compared with the control group, the liver mass and serum levels of ALT, AST, ALP, MDA, NO, TC, TG, HDL-C, LDL-C in the model group were increased significantly (P<0.05, P<0.01), the activities of SOD and GSH-Px were decreased significantly (P<0.05, P<0.01), the liver cells were vacuolated and infiltrated with inflammatory cells, and the expression levels of NF-κB and MAPK protein in liver tissues were increased significantly (P<0.01). Compared with the model group, the levels of ALT, AST, ALP, MDA, NO, TC, TG, HDL-C, LDL-C in Curc group were decreased significantly nd the activities of SOD and GSH-Px were increased significantly (P<0.05, P<0.01). Conclusion: Curc can effectively reduce liver tissue damage by regulating NF-κB/MAPK signal pathway.
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