Inhibitory Effects of Several Spices on Inflammation Caused by Advanced Glycation Endproducts

Abstract

Advanced glycation endproducts (AGEs) is implicated in the pathogenesis of diabetic complications. Inhibiting the formation of AGEs and interfering with AGEs-mediated inflammation are two practicable strategies for developing a dietary adjuvant against diabetic complications. This study evaluated the protective capacities against diabetic complications of several spices based on their inhibition of the formation of AGEs in an in vitro BSA/glucose system and on the AGEs-induced production of proinflammatory cytokine in RAW 264.7 macrophages. Among the tested spices, cinnamon exhibited most strongly inhibited both the formation of AGEs and the AGEs-induced production of nitric oxide, interleukin-6 and tumor necrosis factor-α. Additionally, correlative results revealed that the capacity of spices to inhibit the formation of AGEs is attributable to phenolic compounds and, in contrast, the capacity to inhibit AGEs-induced inflammation is attributable to condensed tannin. This investigation demonstrates the potential of cinnamon to serve as a dietary adjuvant against diabetic complications.

Share and Cite:

S. Ho and P. Chang, "Inhibitory Effects of Several Spices on Inflammation Caused by Advanced Glycation Endproducts," American Journal of Plant Sciences, Vol. 3 No. 7A, 2012, pp. 995-1002. doi: 10.4236/ajps.2012.327118.

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1] M. Brownlee, “Biochemistry and Molecular Cell Biology of Diabetic Complications,” Nature, Vol. 414, 2001, pp. 813-820.
[2] N. Ahmed, “Advanced Glycosylation End Products-Role in Pathology of Diabetic Complications,” Diabetes Research and Clinical Practice, Vol. 67, 2005, pp. 3-21.
[3] R. Clynes, B. Moser, S. F. Yan, R. Ramasamy, K. Herold and A. M. Schmidt, “Receptor for AGE (RAGE): Weaving Tangled Webs Within the Inflammatory Response,” Current Molecular Medicine, Vol. 7, 2007, pp. 743-751.
[4] G. Basta, “Receptor for Advanced Glycation Endproducts and Atherosclerosis: from Basic Mechanisms to Clinical Implications,” Atherosclerosis, Vol. 196, 2008, pp. 9-21.
[5] M. Takeuchi, J.-I. Takino and S.-I. Yamagishi, “Involvement of the Toxic AGEs (TAGE)-RAGE System in the Pathogenesis of Diabetic Vascular Complications: a Novel Therapeutic Strategy,” Current Drug Targets, Vol. 11, 2010, pp. 1468-1482.
[6] K, Srinivasan, “Role of Spices Beyond Food Flavoring: Nutraceuticals with Multiple Health Effects,” Food Reviews International, Vol. 21, 2005, pp. 167-188.
[7] K. Berbaum, K. Shanmugam, G. Stuchbury, F. Wiede, H. Korner and G. Munch, “Induction of Novel Cytokines and Chemokines by Advanced Glycation Endproducts Determined with a Cytometric Bead Array,” Cytokine, Vol. 41, 2008, pp. 198-203.
[8] C.-H. Wu, C.-M. Huang, C.-H. Lin, Y.-S. Ho, C.-M. Chen and H.-M. Lee, “Advanced Glycosylation End Products Induce NF-κB Dependent iNOS Expression in RAW 264.7 Cells,” Molecular and Cellular Endocrinology, Vol. 194, 2002, pp. 9-17.
[9] Y. Okada, M. Okada and Y. Sage-saka, “Screening of Dried Plant Seed Extracts for Adiponectin Production Activity and Tumor Necrosis Factor-alpha Inhibitory Activity on 3T3-L1 Adipocytes,” Plant Foods for Human Nutrition, Vol. 65, 2010, pp. 225-232.
[10] S. Toda, “Antioxidative Effects of Poly-phenols in Leaves of Houttuynia cordata on Protein Fragmentation by Copper-Hydrogen Peroxide in vitro,” Journal of Medicinal Food, Vol. 8, 2005, pp. 266-268.
[11] J. A. Vinson, H. B. Howard III, “Inhibition of Protein Glycation and Advanced Glycation End Products by Ascorbic Acid and Other Vitamins and Nutrients,” Journal of Nutritional Biochemistry, Vol. 7, 1996, pp. 659-663.
[12] Y.-S. Huang and S.-C. Ho, “Poly-methoxy Flavones Are Responsible for the Anti-inflammatory Activity of Citrus Fruit Peel,” Food Chemistry, Vol. 119, 2010, pp.868-873.
[13] R. P. Dear-love, P. Greenspan, D. K. Hartle, R. B. Swanson and J. L. Hargrove, “Inhibition of Protein Glycation by Extracts of Culinary Herbs and Spices,” Journal of Medicinal Food, Vol. 11, No. 2, 2008, pp. 275-281.
[14] X. Peng, K.-W. Cheng, J. Ma, B. Chen, C.-T. Ho, C. Lo, F. Chen and M. Wang, “Cinnamon Bark Proanthocyanidins as Reactive Carbonyl Scavengers to Prevent the Formation of Advanced Glycation Endproducts,” Journal of Agricultural and Food Chemistry, Vol. 56, No. 6, 2008, pp.1907-1911.
[15] M. Saraswat, P. Y. Reddy, P. Muthenna and G. B. Reddy, “Prevention of Non-enzymatic Glycation of Proteins by Dietary Agents: Prospects for Alleviating Diabetic Complications,” British Journal of Nutrition, Vol. 101, 2009, pp.1714-1721.
[16] A. G. Jagtap and P. B. Patil, “Antihyperglycemic Activity and Inhibition of Advanced Glycation End Product Formation by Cuminum cyminum in Streptozotocin Induced Diabetic Rats,” Food and Chemical Toxicology, Vol. 48, 2010, pp. 2030-2036.
[17] P. A. Kumar, P. Y. Reddy, P. N. B. S. Srinivas and G. B. Reddy, “Delay of Diabetic Cataract in Rats by the Antiglycating Potential of Cumin Through Modulation of α-crystallin Chaperone Activity,” Journal of Nutritional Biochemistry, Vol. 20, No. 7, 2009, pp. 553-562.
[18] P.-J. Tsai, T.-H. Tsai, C.-H. Yu and S.-C. Ho, “Evaluation of NO-Suppressing Activity of Several Mediterranean Culinary Spices,” Food and Chemical Toxicology, Vol. 45, 2007, pp. 440-447.
[19] H. S. Lee, B. S. Kim and M. K. Kim, “Suppression Effect of Cin-namomum cassia Bark-Derived Component on Nitric Oxide Synthase,” Journal of Agricultural and Food Chemistry, Vol. 50, 2002, pp. 7700-7703.
[20] N. Bai, K. He, M. Roller, C.-S. Lai, X. Shao, M.-H. Pan and C.-T. Ho, “Flavonoids and Phenolic Compounds from Rosmarinus officinalis,” Journal of Agricultural and Food Chemistry, Vol. 58, 2010, pp. 5363-5367.
[21] V. Hajhashemi, A. Ghannadi and H. Jafarabadi, “Black Cumin Seed Essential Oil, as a Potent Analgesic and Antiinflammatory Drug,” Phytotheraphy Research, Vol. 8, 2004, pp. 195-199.
[22] Z. M. Al-Amin, M. Thomson, K. K. Al-Qattan, R. Peltonen-Shalaby and M. Ali, “Anti-Diabetic and Hypolipidaemic Properties of Ginger (Zingiber officinale) in Streptozotocin-Induced Diabetic Rats,” British Journal of Nutrition, Vol. 96, No. 4, 2006, pp. 660-666.
[23] S. Sharma, S. K. Kulkarni and K. Chopra, “Curcumin, the Active Principle of Turmeric (Curcuma longa), Ameliorates Diabetic Nephropathy in Rats,” Clinical and Experimental Pharmacology and Physiology, Vol. 33, 2006, pp. 940-945.
[24] Y. Shen, M. Fukushima, Y. Ito, E. Muraki, T. Hosono, T. Seki and T. Ariga, “Verification of the Antidiabetic Effects of Cinnamon (Cinnamomum zeylanicum) Using Insulin-Nncontrolled Type 1 Diabetic Rats and Cultured Adipocytes,” Bioscience, Biotechnology, and Biochemistry, Vol. 74, No. 12, 2010, pp. 2418-2425.
[25] P. Suryanarayana, M. Saraswat, T. Mrudula, T. P. Krishna, K. Krishnaswamy and G. B. Reddy, “Curcumin and Turmeric Delay Streptozotocin-Induced Diabetic Cataract in Rats,” Investigative Ophthalmology and Visual Science, Vol. 46, 2005, pp. 2092-2099.
[26] S. Kirkham, R. Akilen, S. Sharma and A. Tsiami, “The Potential of Cinnamon to Reduce Blood Glucose Levels in Patients with Type 2 Diabetes and Insulin Resistance,” Diabetes Obesity and Metabolism, Vol. 11, No. 12, 2009, pp. 1100-1113.

Copyright © 2024 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.