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Evaluation of Antiglycation Effects of Extracts Obtained from Canarium album Raeusch Fruit and Beneficial Activity on Advanced Glycation Endproduct-Mediated Oxidative Stress and Inflammation in Monocytes and Vascular Endothelial Cells

Authors: Chiung-Tsun Kuoa, Tzu-Hao Liu, Fang-Yi Lin, Tai-Hao Hsu, Hui-Yin Chen


Hyperglycemia-mediated accumulation of advanced glycation end-products (AGEs) play a pivotal role in the development of diabetic complications by inducing inflammation. In the present study, we evaluated the possible effects of water/ethanol (1/1, v/v) extracts (WEE) and its fractions from Canarium album Raeusch. (Chinese olive) which is a fruit used on AGEs-stimulated oxidative stress and inflammation in monocytes and vascular endothelial cells. Co-incubation of EA.hy926 endothelial cells with WEE and its fractions for 24h resulted in a significant decrease of monocyte–endothelial cell adhesion, the expression of ICAM-1, generation of intracellular ROS and depletion of GSH induced by AGEs. Chinese olive fruit extracts also reduced the expression of pro-inflammatory mediates, such as TNF-α, IL-1β and IL-6 in THP-1 cells. These findings suggested that Chinese olive fruit was able to protect vascular endothelium from dysfunction induced by AGEs. 

Keywords: Inflammation, endothelial dysfunction, Advanced glycation end-products (AGEs), Canarium album Raeusch

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[1] J. E Shaw, R. A. Sicree, P. Z. Zimmet, “Global estimates of the prevalence of diabetes for 2010 and 2030,”Diabetes Res. Clin. Pract., vol. 87, pp. 4-14,2010.
[2] N. Ahmed, “Advanced glycation endproducts-role in pathology of diabetic complications, ”Diab. Res. Clin. Pract., vol 67, pp.3–21, 2005.
[3] S. Pennathur, J. W. Heinecke, “Mechanisms for Oxidative Stress in Diabetic Cardiovascular Disease, ”Antioxidants & Redox Signaling, vol.9, no.7, pp. 955-969, 2007.
[4] R. Madonna, R. De Caterina.“Cellular and molecular mechanisms of vascular injury in diabetes—part I: pathways of vascular disease in diabetes,”Vascul. Pharmacol., vol. 54, no. 3–6, pp. 68–74, 2011.
[5] G. Basta, A. M. Schmidt, R. De Caterina, “Advanced glycation end products and vascular inflammation: implications for accelerated atherosclerosis in diabetes, ”Cardiovasc. Res.vol. 63,no. 4,pp.582-592, 2004.
[6] R. Ramasamy, S. J. Vannucci, S. S. Yan, K. Herold, S. F. Yan and A. M. Schmidt, “Advanced glycation end products and RAGE: a common thread in aging, diabetes, neurodegeneration, and inflammation, ”Glycobiol. vol. 15 no. 7, pp. 16R–28R, 2005.
[7] J. E. Deanfield, J. P. Halcox, and T. J. Rabelink, “Endothelial function and dysfunction, ”Circulation. vol. 115, pp.1285-1295, 2007.
[8] Orasanu, G. and J. Plutzky, “The pathologic continuum of diabetic vascular disease, ”J. Am. Coll. Cardiol. vol. 53 no.5s1, pp. S35-S42, 2009.
[9] N. R. Madamanchi, and M. S. Runge, “Mitochondrial dysfunction in atherosclerosis, ”Circulation Res.vol. 100, pp. 460-473, 2007.