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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.2014011320
pages 205-218

Curative Effect of Amorphophallus campanulatus (Roxb.) Blume. Tuber On N-Nitrosodiethylamine- Induced Hepatocellular Carcinoma in Rats

Puthuparampil Nazarudeen Ansil
Biochemistry and Pharmacognosy Research Laboratory, School of Biosciences, Mahatma Gandhi University, P.D. Hills. P.O, Kottayam, Kerala, India
Anand Nitha
Biochemistry and Pharmacognosy Research Laboratory, School of Biosciences, Mahatma Gandhi University, P.D. Hills. P.O, Kottayam, Kerala, India
Santhibhavan Prabhakaran Prabha
Biochemistry and Pharmacognosy Research Laboratory, School of Biosciences, Mahatma Gandhi University, P.D. Hills. P.O, Kottayam, Kerala, India
Mukalel Sankunni Latha
Biochemistry and Pharmacognosy Research Laboratory, School of Biosciences, Mahatma Gandhi University, P.D. Hills. P.O, Kottayam, Kerala, India

SINOPSIS

In this study, we investigated the curative effect of Amorphophallus campanulatus tuber methanolic extract (ACME) on N-nitrosodiethylamine (NDEA)−induced hepatocellular carcinoma (HCC) in experimental rats. All of the rats except those in the normal control group received 0.02% NDEA orally (2 mL, 5 days/week) for the first 20 weeks of the experiment. In different treatment groups, after 20 weeks of NDEA challenge, rats were supplemented with ACME (125 and 250 mg/kg body weight, orally) for the following 28 days. In addition, a standard drug control group was supplemented with silymarin (100 mg/kg bw, orally), a known tumorsuppressive agent against HCC. Administration of ACME significantly inhibited the NDEA-induced increase of hepatic nodule incidence, nodule multiplicity, and serum biochemical indices, and improved the hepatocellular architecture in a dose-dependent manner. The biochemical analysis of hepatic tissues further demonstrated that ACME counteracts NDEA-induced oxidative stress through the restoration of antioxidant enzymes. NDEAadministered rats also showed amplified expression of proliferating cell nuclear antigen in the liver, and decreased expression of this proliferative marker was clearly observed upon the supplementation of ACME. Notably, 250 mg/kg bw ACME supplementation showed better results than the other treatment regimens; this result might be associated with the enhancement of antioxidant activity and inhibition of hepatic cell proliferation.


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