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ORIGINAL ARTICLE
Year : 2018  |  Volume : 14  |  Issue : 54  |  Page : 186-190

Biochemical evidence for the antitumor potential of Garcinia mangostana Linn. On diethylnitrosamine-induced hepatic carcinoma


1 Department of Biochemistry, Saveetha Dental College and Hospital, Saveetha University, Velappanchavadi, Chennai, Tamil Nadu, India
2 Department of Biochemistry, Biogen Care Research Center, Chennai, Tamil Nadu, India
3 Department of Biochemistry, College of Medicine, Texila American University, Guyana, South America

Correspondence Address:
Mallika Jainu
Department of Biochemistry, Biogen Care Research Center, 32/285, Royapettah High Road, Chennai - 600 014, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/pm.pm_213_17

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Background: Garcinia mangostana is extensively used in most of the Indian herbal pharmaceuticals and nutraceuticals. Objective: The objective of this study was to elucidate the underlying biochemical protective mechanism of G. Mangostana Linn. fruit extract (GME) in deterioration of diethylnitrosamine (DEN)-induced hepatic carcinoma (HCC) in rats. Materials and Methods: The cancer was induced using DEN to the experimental rats and treated with GME (200, 400, and 600 mg/kg) to find its anticancer property. The cancer biomarkers such as alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA), hepatic hydroxyl proline, total tissue protein, and tumor necrosis factor-alpha levels were measured using ELISA. The vascular endothelial growth factor expressions were also seen in liver tissues using immunohistochemistry. Results: In addition, there was a significant increase in serum AFP, CEA, hepatic hydroxylproline, and total tissue protein levels in HCC group versus the negative control group. In contrast, the groups with HCC subjected to either high or low dose of GME elicited significant reduction of AFP, CEA, hepatic hydroxylproline, and increase in total protein in serum compared to the untreated HCC rats. Interestingly, treatment with GME elicited marked improvement in the liver histological feature and downregulation of tumor necrosis factor-alpha levels in HCC groups. GME extract may have chemopreventive benefits by reducing the tumor promoting growth factor levels in HCC-induced group. Conclusion: To sum up, all findings on curative groups had proved clearly that the GME has anticarcinogenic effect on the development of liver cancer induced by DEN in rats. Abbreviations used: TNF-α: Tumor necrosis factor-alpha, PBS: Phosphate buffered saline, ROS: Reactive oxygen species, DNA: Deoxyribonucleic acid, GSH: Glutathione, VEGF: Vascular endothelial growth factor.


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