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Antiproliferative effect of rhein, an anthraquinone isolated from Cassia species, on Caco-2 human adenocarcinoma cells.

Biomedical Sciences Research Institute Computer Science Research Institute Environmental Sciences Research Institute Nanotechnology & Advanced Materials Research Institute

Aviello , Gabriella, Rowland, Ian, Gill, Chris, Acquaviva , Angela Maria, Capasso , Francesco, Mccann, Mark, Capasso , Raffaele, Izzo , Angelo A. and Borrelli , Francesca (2009) Antiproliferative effect of rhein, an anthraquinone isolated from Cassia species, on Caco-2 human adenocarcinoma cells. Journal of Cellular amd Molecular Medicine, . . [Journal article]

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DOI: 10.1111/j.1582-4934.2009.00815.x

Abstract

In recent years the use of anthraquinone laxatives, in particular senna, has been associated with damage to the intestinal epithelial layer and an increased risk of developing colorectal cancer. In the present study we evaluated the cytotoxicity of rhein, the active metabolite of senna, on human colon adenocarcinoma cells (Caco-2) and its effect on cell proliferation. Methods: Cytotoxicity studies were performed using MTT, NR and TEER assays whereas (3)H-thymidine incorporation and western blot analysis were used to evaluate the effect of rhein on cell proliferation. Moreover, for genoprotection studies Comet assay and oxidative biomarkers measurement (malondialdehyde and reactive oxygen species) were used. Results: Rhein (0.1-10mug/ml) had no significant cytotoxic effect on proliferating and differentiated Caco-2 cells. Rhein (0.1 and 1 mug/ml) significantly reduced cell proliferation as well as MAP kinase activation; by contrast, at the high concentration (10mug/ml) rhein significantly increased cell proliferation and ERK phosphorylation. Moreover, rhein (0.1-10mug/ml) (i) did not adversely affect the integrity of tight junctions and hence epithelial barrier function, (ii) did not induce DNA damage rather it was able to reduce H(2)O(2)-induced DNA damage and (iii) significantly inhibited the increase in malondialdehyde and ROS levels induced by H(2)O(2)/Fe(2+). Conclusions: Rhein, was devoid of cytotoxic and genotoxic effects in colon adenocarcinoma cells. Moreover, at concentrations present in the colon after a human therapeutic dosage of senna, rhein inhibited cell proliferation via a mechanism which seems to involve directly the MAP kinase pathway. Finally, rhein prevents the DNA damage probably via an anti-oxidant mechanism

Item Type:Journal article
Faculties and Schools:Faculty of Life and Health Sciences
Faculty of Life and Health Sciences > School of Biomedical Sciences
Research Institutes and Groups:Biomedical Sciences Research Institute
Biomedical Sciences Research Institute > Northern Ireland Centre for Food and Health (NICHE)
ID Code:3919
Deposited By:Dr Chris Gill
Deposited On:17 Dec 2009 15:09
Last Modified:11 Feb 2010 15:05

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