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Coordinación General de Investigación de la Facultad de Salud Pública y Nutrición y la Dirección General de Sistemas e Informática de la Universidad Autónoma de Nuevo León

2017, Number 2

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Rev Salud Publica Nutr 2017; 16 (2)

Incremento de la expresión de TLR4 y efecto antioxidante del ácido acetilsalicílico en conejos con dieta alta en grasas

Ortíz-Reyes AE, Calderón-Torres CM

Language: Spanish
References: 37
Page: 1-10
PDF size: 384.84 Kb.


ABSTRACT

Introduction: The obesity and liver diseases progression are characterized by the increase and accumulation of lipids in tissues and blood, inflammation and oxidative stress. These diseases are now a worldwide epidemic, and the number of young people affected is increasing in the Mexican population. This increase has led to medical research towards the early detection of the metabolic syndrome, which is used as an indicator of symptoms that may be at risk for health and lead to liver disease. Objective: The objectives of the present study were to evaluate in a model of dyslipidemia in young rabbits fed three months with a diet high in fat (20% palmitic acid), the production of reactive oxygen species and changes in TLR4, COX2 and IL-1β gene expression, as markers of inflammation and oxidative stress; also to evaluate the effect of acetylsalicylic acid on the production of free radicals and on the expression of these genes. Results: In rabbits fed with excess of fat, significantly increased the levels of triglycerides (p‹0.05), TLR4 expression, and reactive oxygen species, although in the latter, not significantly. The administration of acetylsalicylic acid in anti-inflammatory doses decreased the production of reactive oxygen species and the expression of TLR4. Discussion: The high fat intake in young rabbits lead to dyslipidemia and overexpression of TLR4, a key gene in the inflammatory response and linked to the increase of reactive oxygen species. The results indicate that acetylsalicylic acid has an antioxidant effect


REFERENCES

  1. Akarasereenont P, Bakhle YS, Thiemermann C y Vane JR. (1995). Cytokine-mediated induction of cyclooxygenase- 2 by activation of tyrosine kinase in bovine endothelial cells stimulated by bacterial lipopolysaccharide. British Journal of Pharmacology; 115: 401-408.

  2. Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman J, Donato KA, Fruchart J, James W, Loria CM, Smith SC Jr. International Diabetes Federation Task Force on Epidemiology and Prevention, National Heart, Lung, and Blood Institute, American Heart Association, World Heart Federation, International Atherosclerosis Society, International Association for the Study of Obesity. (2009). Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation 120: 1640–1645.

  3. Ayyadevara S, Bharill P, Dandapat A, Hu C, Khaidakov M, Mitra S, Shmooklwe Reis RJ y Mehta JL. (2013). Aspirin Inhibits Oxidant Stress, Reduces Age- Associated Functional Declines, and Extends Lifespan of Caenorhabditis elegans. Antioxidants & Redox Signaling; 18 (5):481-490.

  4. Battaglia V, Salvi M y Toninello A. (2005). Oxidative stress is responsible for mitochondrial permeability transition induction by salicylate in liver mitochondria. Journal of Biological Chemistry; 280(40): 33864- 33872.

  5. Calderón M, Peña A y Thomé PE. (2006). DhARO4, an amino acid biosynthetic gene, is stimulated by high salinity in Debaryomyces hansenii. Yeast; (23):725– 734.

  6. Cardoso AR, Kakimoto PA y Kowaltowski AJ. (2013). Diet-Sensitive Sources of Reactive Oxygen Species in Liver Mitochondria: Role of Very Long Chain Acyl- CoA Deshydrogenases. PLOS ONE; 8 (10): e77088.

  7. Clària J, Lee MH y Serhan CN. (1996). Aspirin-Triggered Lipoxins (15-epi-LX) Are Generated by the Human Lung Adenocarcinoma Cell Line (A549)- Neutrophil Interactions and Are Potent Inhibitors of Cell Proliferation. Molecular Medicine; 2(5):583-596.

  8. Cyrus T, Sung S, Zhao L, Funk CD, Tang S y Praticò D. (2002). Effect of Low-Dose Aspirin on Vascular Inflammation, Plaque Stability, and Atherogenesis in Low Density Lipoprotein Receptor-Deficient Mice. Circulation; 106:1282-1287.

  9. Chen S, Lin G, Lei L, You X, Wu C, Xu W, Huang M, Luo L, Wang Z, Li Y, Zhao X, y Yan F. (2013). Hyperlipidemia Modifies Innate Immune Responses to Lipopolysaccharide via the TLR-NF-κB Signaling Pathway. Inflammation; 36(4): 968-976.

  10. Fang D, Yang S, Quan W, Jia H, Quan Z y Qu Z. (2014). Atorvastatin suppresses Toll-like receptor 4 expression y NF-kB activation in rabbit atherosclerotic plaques. European Review for Medical and Pharmacological Sciences; (18): 242-246.

  11. Fields M, Lewis CG y Bureau I. (2001). Aspirin Reduces Blood Cholesterol in Copper-Deficient Rats: A Potential Antioxidant Agent? Metabolism; 50(5): 558- 561.

  12. Furukawa S, Fujita T, Shimabukuro M, Iwaki M, Yamada Y, Nakajima Y, Nakayama O, Makishima M, Matsuda M, y Shimomura I. (2004). Increased oxidative stress in obesity and its impact on metabolic syndrome. J Clin Invest; 114(12):1752-1761.

  13. Gou J y Friedman SL. (2010). Toll-like receptor 4 signaling in liver injury and hepatic fibrogenesis. Fibrogenesis & Tissue Repair; (3):21.

  14. Hempel SL, Buettner GR, O´Malley YQ, Wessels DA, y Flaherty DM. (1999). DihydrofluoresceinDiacetate is superior for detecting intracellular oxidants: Comparision with 2’7’ Dichlorodihydrofluorescein diacetate, 5 (and 6)-Carboxy-2’7’ Dichlorodihydrofluorescein diacetate and Dihydrorhodamine 123. Free Radical Biology & Medicine; 27(1-2): 146–159.

  15. Hsieh PS, Jin JS, Chiang CF, Chan PC, Chen CH y Shih KC. (2009). COX-2-mediated Inflammation in Fat Is Crucial for Obesity-linked Insulin Resistance and Fatty Liver. Obesity; (17): 1150–1157.

  16. Integrated DNA Technologies. (2017). www.idtdna.com/pages. Obtenido de https://www.idtdna.com/calc/analyzer

  17. Kibbe, W. (2007). OligoCalc: an online oligonucleotide properties calculator. Obtenido de http://biotools.nubic.northwestern.edu/OligoCalc.html

  18. Kourtis N y Tavernarakis N. (2011). Cellular stress response pathways and ageing: intricate molecular relationships. EMBO Journal; (30): 2520–2531.

  19. Lee JY, Ye J, Gao Z, Youn H, Lee WH, Zhao L, Sizemore N y Hwang DH. (2003). Reciprocal Modulation of Toll-like Receptor-4 Signaling Pathways Involving MyD88 and Phosphatidylinositol 3-Kinase/AKT by Saturated and Polyunsaturated Fatty Acids. The Journal of Biological Chemistry; 278 (39): 37041– 37051.

  20. Liu J, Zhuang ZJ, Bian D, Ma XJ, Xun YH, Yang WJ, Lou Y, Liu YL, Jia L, Wang Y, Zhu M, Ye DW, Zhou G, Lou GQ y Shi JP. (2014). Toll-like receptor-4 signalling in the progression of non-alcoholic fatty liver disease induced by high-fat and high-fructose diet in mice. Clinical and Experimental Pharmacology and Physiology; (41):482-488.

  21. Mahmood KA, Ahmed JH y Jawad AM. (2009). Nonstereroidal anti-inflammatory drugs (NSAIDS), free radicals and reactive oxygen species (ROS): A review of literature. The Medical Journal of Basrah University; 27(1):46-53.

  22. Manček-Keber M, Frank-Bertoncelj M, Hafner-Bratkovič I, Smole A, Zorko M, Pirher N, Hayer S, Kralj-Iglič V, Rozman B, Ilc N, Horvat S y Jerala R. (2015). Toll-like receptor 4 senses oxidative stress mediated by the oxidation of phospholipids in extracellular vesicles. Science Signaling; 8(381): 1-12.

  23. McRae MP. (2008). Vitamin C supplementation lowers serum low-density lipoprotein cholesterol and triglycerides: a meta-analysis of 13 randomized controlled. Journal of Chiropractic Medicine; (7); 48– 58.

  24. Milagro FI, Javier Campión J, y Martínez JA. (2006). Weight Gain Induced by High-Fat Feeding Involves Increased Liver Oxidative Stress. Obesity; 14(7): 1118-1123.

  25. Oliveira CP, da Costa Gayotto LC, Tatai C, Della Bina BI, Janiszewski M, Lima ES, Abdalla DS, Lopasso FP, Laurindo FR y Laudanna AA. (2002). Oxidative stress in the pathogenesis of nonalcoholic fatty liver disease, in rats fed with a choline-deficient diet. J Cell Mol Med; 6 (3): 399-406.

  26. Pagadala M, Zein CO y McCullough AJ. (2009). Predictors of Steatohepatitis and Advanced Fibrosis in Non- Alcoholic Fatty Liver Disease. Clin Liver Dis; (13): 591–606.

  27. Paul-Clark MJ, Van Cao T, Moradi-Bidhendi N, Cooper D y Gilory DW. (2004). 15-epi-lipoxin A4-mediated Induction of Nitric Oxide Explains How Aspirin Inhibits Acute Inflammation. J Expe Med; 200(1):69- 78.

  28. Petrosillo G, Portincasa P, Grattagliano I, Casanova G, Matera M, Ruggiero FM, Ferri y Paradies G. (2007). Mitochondrial dysfunction in rat with nonalcoholic fatty liver Involvemet of complex I, reactive oxygen species and cardiolipin. Biochimica et Biophysica Acta; (1726):1260-1267.

  29. Podhaisky HP, Abate A, Polte T, Oberle OS y Schröder H. (1997). Aspirin protects endothelial cells from oxidative stress - possible synergism with vitamin E. FEBS Letters; (417): 349-351.

  30. Ricciotti E y FitzGerald GA. (2011). Prostaglandins and Inflammation. Arterioscler Thromb Vasc Biol; 31(5): 986-1000.

  31. Schmitt ME, Brown TA y Trumpower BL (1990) A rapid and simple method for preparation of RNA from Saccharomyces cerevisiae. Nucleic Acids Res; (18):3091-3092.

  32. Song J, Ke SF, Zhou CC, Zhang SL, Guan YF, Xu TY, Sheng CQ, Wang P y Miao CY. (2013). Nicotinamide Phosphoribosyltransferase Is Required for the Calorie Restriction–Mediated Improvements in Oxidative Stress, Mitochondrial Biogenesis, and Metabolic Adaptation. J Gerontol A Biol Sci Med Sci; 69(1):44– 57.

  33. Stojsavljević S, Gomerčić Palčić M, Virović Jukić L, Smirčić Duvnjak L y Duvnjak M. (2014). Adipokines and proinflammatory cytokines, the key mediators in the pathogenesis of nonalcoholic fatty liver disease. World Journal of Gastroenterology; 20(28):18070- 18091.

  34. Suganami T, Tanimoto-Koyama K, Nishida J, Itoh M, Yuan X, Mizuari S, Kotani H, Yamaoka S, Miyake K, Aoe S, Kamei Y y Ogawa Y. (2007). Role of the Tolllike Receptor 4/NF-kappaB Pathway in Saturad Fatty Acid-Induced Inflammatory Changes in the Interaction Between Adipocytes and Macrophages. Arterioscler Thromb Vasc Biol. 27(1):84-91. DOI: 10.1161/01

  35. Tilg H. (2010). The Role of Cytokines in Non-Alcoholic Fatty Liver Disease. Digestive Diseases; 28(1): 179- 185.

  36. Untergasser A, C. K.-S. (2012). Primer3-new capabilities and interfaeces. Obtenido de bioinfo.ut.ee: http://bioinfo.ut.ee/primer3-0.4.0/

  37. Yu J, Ip E, De la Peña A, Hou JY, Sesha J, Pera N, Hall P, Kirsh R, Leclerq I y Farrell C. (2006). COX-2 Induction in Mice With Experimental Nutritional Steotohepatitis: Role as Pro-inflammatory Mediator. Hepatology; 43(4): 286-386.




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