Abstract
The current study was designed to investigate the effect of Citrus limon. (L.) Burm. (Rutaceae) fruits, commonly known as lemon, in experimental liver damage. The ethanol extract of Citrus limon. fruits was evaluated for its effects on experimental liver damage induced by carbon tetrachloride, and the ethyl acetate soluble fraction of the extract was evaluated on HepG2 cell line. The ethanol extract normalized the levels of aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT), alkaline phosphatase (ALP), and total and direct bilirubin, which were altered due to carbon tetrachloride intoxication in rats. In the liver tissue, treatment significantly reduced the levels of malondialdehyde (MDA), hence the lipid peroxidation, and raised the levels of antioxidant enzymes superoxide dismutase (SOD) and catalase. It improved the reduced glutathione (GSH) levels in treated rats in comparison with CCl4-intoxicated rats. In the histopathologic studies, treated animals exhibited restoration of the liver architecture toward normal. Three doses of ethanol extract (i.e., 150, 300, and 500 mg/kg) were evaluated. The effect seen was dose dependent, and the effect of the highest dose was almost equal to the standard silymarin. In the investigation carried out on human liver–derived HepG2 cell line, significant reduction in cell viability was observed in cells exposed to CCl4. A dose-dependent increase in the cell viability was observed when CCl4-exposed HepG2 cells were treated with different concentrations of ethyl acetate soluble fraction of the ethanol extract. The highest percentage viability of HepG2 cells was observed at a concentration of 100 µg/mL. The extract merits further investigation to identify the active principles responsible for the hepatoprotective effect. The results from the current investigation also indicate good correlation between the in vivo. and in vitro. studies.
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