Objective: To observe the histological and biochemical alterations that may occur in the liver tissue of rat by ethanol intoxication and to investigate the role of Ginger supplementation against these alterations.
Study design: Experimental study.
Place & duration of study: Department of morbid anatomy and Histopathology, University of health sciences Lahore from January to December 2016.
Materials and methods: Thirty rats were divided into three Groups 1, Group 2, and Group 3. Group 1 which was a negative control group, was kept on normal routine diet. Group 2, positive control was fed with 5% w/w Alcohol (Ethanol). Group 3 which was experimental group was fed with Ginger 100mg/kg body weight thrice a week in addition to Alcohol. Experiment continued for four weeks. Blood samples were taken at day 0 and 29 at the end of experiment. Serum parameters and liver histopathology was done before and after the end of experiment to see Hepatic lobular architecture, Hepatocyte morphology, Inflammation, Stromal reaction, Steatosis, Central vein and Fibrosis.
Results: Positive control group 2 animals showed significant alteration in the liver histology due to Alcohol intoxication as compared to negative control group 1 animals. Experimental group 3 showed abrogation of toxic effects induced by Alcohol intoxication. Similarly, positive control group 2 revealed significant elevation in the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and triglycerides (TG). Serum levels of low density lipoprotein (LDL) Cholesterol was significantly reduced in G 2 animals. Experimental group G3 animals showed significant reduction in serum levels of ALT, AST and TG. There was no significant difference in serum LDL cholesterol level of Group 3 as compared to positive control group 2.
Conclusion: Alcohol (Ethanol) induces liver parenchymal injury in the form of inflammation, distortion of hepatic lobular architecture and fatty change in the rat liver. Herbal supplement has hepatoprotective effect against hepatotoxicity induced by Alcohol.Key words: Alcohol, Alcoholic hepatitis, Steatosis, Luteolin.