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Journal of Environmental Pathology, Toxicology and Oncology
Factor de Impacto: 1.625 Factor de Impacto de 5 años: 1.63 SJR: 0.402 SNIP: 0.613 CiteScore™: 2.3

ISSN Imprimir: 0731-8898
ISSN En Línea: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.2014011354
pages 295-314

Inhibition of Hep G2 Hepatic Cancer Cell Growth and CCl4 Induced Liver Cytotoxicity in Swiss Albino Mice by Mahua Extract

Sudipta Ray
Department of Signal Transduction and Biogenic Amines, Chittaranjan National Cancer Institute, Kolkata, India
Murmu Nabendu
Department of Signal Transduction and Biogenic Amines, Chittaranjan National Cancer Institute, Kolkata, India
Jyotirmay Adhikari
Department of Translation Research, Chittaranjan National Cancer Institute, Kolkata, India
Sayantan Bhattacharyya
Department of Signal Transduction and Biogenic Amines, Chittaranjan National Cancer Institute, Kolkata, India
Sumanto Adhikari
Department of Translation Research, Chittaranjan National Cancer Institute, Kolkata, India
Samir Banerjee
Department of Signal Transduction and Biogenic Amines, Chittaranjan National Cancer Institute, Kolkata, India

SINOPSIS

Mahua flower extract may provide protective effects against hepatotoxicity. The effect of Mahua flower extract (ME) was investigated on Hep G2 cell line and carbon tetrachloride (CCl4)-induced liver damages in Swiss albino mice. To investigate its cytotoxic effect in liver cancer, Hep G2 cells were treated with different doses of ME, and cell proliferation as well as colony formation assays demonstrated dose-dependent cytotoxicity of ME towards Hep G2 cells in tissue culture. Further gene expression studies showed significant down-regulation of AKT1/2/3, p-AKT, and COX-2 proteins including up-regulation of active caspase-3 in ME treated Hep G2 cells. In in vivo experiments, the mice were pretreated with ME for 15 days. On the 16th day CCl4 was injected intraperitoneally and after 24 h all mice were sacrificed. The antioxidant enzyme activities were measured in liver homogenates. CCl4-induced hepatotoxicity was evidenced by significant increase in lipid peroxidation and decrease in activities of antioxidant enzymes such as GST, GSH, SOD, CAT, and GPx. Histological studies showed CCl4-induced centrilobular necrosis and formation of fatty vacuoles in cirrhotic mice liver. Treatment with ME at a dose of 2 mg and 4 mg/kg exhibited the potential to prevent significant liver toxicity. The expression of active caspase-3 protein was down-regulated in ME treated groups compared to CCl4 exposed animals. This study demonstrated ME mediated antioxidant activity and hepatoprotective effects; therefore it could be used in the future for treating hepatic disorders including liver cancer, especially in combination with chemotherapeutics.


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