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The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat
Published on: June 17, 2016
Ameliorative Effects of Lycopene and L-Carnitine on CCl4-Induced Liver Fibrosis Rat Model
Adeel Shahid1, Somia Shehzadi1, Moazzam Salamat1
1University Institute of Medical Laboratory Technology The University of Lahore Lahore Pakistan.
Abstract:
Liver toxicity is a major health concern caused by pharmaceutical exposure, poisons like CCl4, or environmental contaminants. The CCl4-induced liver toxicity model is extensively used to study hepatic damage, such as oxidative stress and fibrosis. In current study, synergistic effect of natural compounds Lycopene (Lyc) and L-Carnitine (L-Car) possessing the antioxidant activity was assessed to mitigate the liver fibrosis induced by CCl4 in male rat model. CCl4 treated rats showed significant decrease in body weight (21.62% ± 0.83%) alongside elevated liver enzymes ALP (276 ± 6.62), AST (283 ± 4.53), ALT (138 ± 0.74), bilirubin (1.73 ± 0.74) and lactate dehydrogenase (LDH) an injury marker (0.778% ± 0.06%). After treatment of CCl4 induced fibrosis with Lyc + L-Car, significantly increased body weight of rats was observed (34.39% ± 0.77%). Liver enzymes also showed remarkable improvement after treatment with Lyc + L-Car (p ≤ 0.001). Combined Lyc + L-Car group showed reduced the LDH level (0.246% ± 0.02%), fibrosis gene markers TIMP-1 and Col1α1 (p ≤ 0.001) and increased antioxidant enzyme activity of SOD (0.56 ± 0.04 U/dL) and CAT (0.489 ± 0.004 U/dL). Histological analysis showed a marked improvement in liver architecture, with reduced fibrosis appearance. These findings suggest that combination of Lyc and L-Car supplementation effectively counteracts fibrosis, oxidative stress, and liver enzymes elevation, supporting its potential role as a dietary therapeutic agent for metabolic and hepatic disorders. Future recommendations include conducting long- term clinical trials in humans to validate these findings, exploring optimal dosages for dietary lycopene supplementation, and investigating its molecular mechanisms of action.

