Caffeic Acid Phenethyl Ester: Consequences of Its Hydrophobicity in the Oxidative Functions and Cytokine Release by Leukocytes

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art_PARACATU_Caffeic_Acid_Phenethyl_Ester_Consequences_of_Its_Hydrophobicity_2014.PDF (1.89 MB)
Citações na Scopus
15
Tipo de produção
article
Data de publicação
2014
DOI
Scopus
Web of Science
Título da Revista
ISSN da Revista
Título do Volume
Editora
HINDAWI PUBLISHING CORPORATION
Autores
PARACATU, Luana Chiquetto
FARIA, Carolina Maria Quinello Gomes
ZERAIK, Maria Luiza
FONSECA, Luiz Marcos da
XIMENES, Valdecir Farias
Citação
EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE, article ID 793629, 13p, 2014
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Numerous anti-inflammatory properties have been attributed to caffeic acid phenethyl ester (CAPE), an active component of propolis. NADPH oxidases are multienzymatic complexes involved in many inflammatory diseases. Here, we studied the importance of the CAPE hydrophobicity on cell-free antioxidant capacity, inhibition of the NADPH oxidase and hypochlorous acid production, and release of TNF-alpha and IL-10 by activated leukocytes. The comparison was made with the related, but less hydrophobic, caffeic and chlorogenic acids. Cell-free studies such as superoxide anion scavenging assay, triene degradation, and anodic peak potential (E-pa) measurements showed that the alterations in the hydrophobicity did not provoke significant changes in the oxidation potential and antiradical potency of the tested compounds. However, only CAPE was able to inhibit the production of superoxide anion by activated leukocytes. The inhibition of the NADPH oxidase resulted in the blockage of production of hypochlorous acid. Similarly, CAPE was the more effective inhibitor of the release of TNF-alpha and IL-10 by Staphylococcus aureus stimulated cells. In conclusion, the presence of the catechol moiety and the higher hydrophobicity were essential for the biological effects. Considering the involvement of NADPH oxidases in the genesis and progression of inflammatory diseases, CAPE should be considered as a promising anti-inflammatory drug.
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https://observatorio.fm.usp.br/handle/OPI/9204
Referências
  1. Baliga MS, 2012, FOOD FUNCT, V3, P1109, DOI 10.1039/c2fo30097d
  2. Barbacanne MA, 2000, FREE RADICAL BIO MED, V29, P388, DOI 10.1016/S0891-5849(00)00336-1
  3. Barth BM, 2012, CELL SIGNAL, V24, P1126, DOI 10.1016/j.cellsig.2011.12.020
  4. Bergman M, 2010, HEART VESSELS, V25, P426, DOI 10.1007/s00380-009-1204-8
  5. BRANDWILLIAMS W, 1995, FOOD SCI TECHNOL-LEB, V28, P25
  6. Cakir T, 2011, J PHARM PHARMACOL, V63, P1566, DOI 10.1111/j.2042-7158.2011.01359.x
  7. Celli N, 2004, J CHROMATOGR B, V810, P129, DOI 10.1016/j.jchromb.2004.07.024
  8. Chen F, 2013, CNS NEUROSCI THER, V19, P675, DOI 10.1111/cns.12131
  9. Ciz M, 2012, OXID MED CELL LONGEV, DOI 10.1155/2012/181295
  10. Csiszar A, 2008, J APPL PHYSIOL, V105, P1333, DOI 10.1152/japplphysiol.90470.2008
  11. Cui KQ, 2013, BIOCHEM BIOPH RES CO, V435, P289, DOI 10.1016/j.bbrc.2013.04.026
  12. Dale DC, 2008, BLOOD, V112, P935, DOI 10.1182/blood-2007-12-077917
  13. Dang PMC, 2006, FASEB J, V20, P1504, DOI 10.1096/fj.05-5395fje
  14. de Almeida A. C., 2012, ISRN INFLAMMATION, V2012
  15. de Almeida AC, 2011, EUR J PHARMACOL, V660, P445, DOI 10.1016/j.ejphar.2011.03.043
  16. de Faria CMQG, 2012, CURR MED CHEM, V19, P4885
  17. Dewas C, 2003, J IMMUNOL, V171, P4392
  18. dos Santos JS, 2013, J BURN CARE RES, V34, P682, DOI 10.1097/BCR.0b013e3182839b1c
  19. Drummond GR, 2011, NAT REV DRUG DISCOV, V10, P453, DOI 10.1038/nrd3403
  20. ENGLISH D, 1974, J IMMUNOL METHODS, V5, P249, DOI 10.1016/0022-1759(74)90109-4
  21. Fischer MT, 2012, BRAIN, V135, P886, DOI 10.1093/brain/aws012
  22. Gebhard C, 2013, BIOL PHARM BULL, V36, P1032
  23. GHOSE AK, 1987, J CHEM INF COMP SCI, V27, P21, DOI 10.1021/ci00053a005
  24. Gunckel S, 1998, CHEM-BIOL INTERACT, V114, P45, DOI 10.1016/S0009-2797(98)00041-6
  25. Huang Y, 2012, J HUAZHONG U SCI-MED, V32, P642, DOI 10.1007/s11596-012-1011-9
  26. Juman S, 2012, BIOL PHARM BULL, V35, P1941
  27. Kettle A. J., 2013, BIOCHIM BIOPHYS ACTA, V1840, P781
  28. Khalil Mahmoud Lotfy, 2006, Asian Pac J Cancer Prev, V7, P22
  29. Kleniewska P, 2012, ARCH IMMUNOL THER EX, V60, P277, DOI 10.1007/s00005-012-0176-z
  30. Laguerre M, 2008, ANAL BIOCHEM, V380, P282, DOI 10.1016/j.ab.2008.06.006
  31. Lin CJ, 2012, CELL BIOL INT, V36, P391, DOI 10.1042/CBI20110290
  32. Lojek A, 2002, LUMINESCENCE, V17, P1, DOI 10.1002/bio.664
  33. Long T, 2012, J SEX MED, V9, P1801, DOI 10.1111/j.1743-6109.2012.02739.x
  34. Munoz A, 2013, OXIDATIVE MED CELLUL, V2013
  35. Natarajan K, 1996, P NATL ACAD SCI USA, V93, P9090, DOI 10.1073/pnas.93.17.9090
  36. ODONNELL VB, 1993, BIOCHEM J, V290, P41
  37. Pečivová Jana, 2012, Interdiscip Toxicol, V5, P81, DOI 10.2478/v10102-012-0014-5
  38. Petronio MS, 2013, MOLECULES, V18, P2821, DOI 10.3390/molecules18032821
  39. Philippens IHCHM, 2013, J NEUROIMMUNE PHARM, V8, P715, DOI 10.1007/s11481-013-9450-z
  40. Pramanik KC, 2013, CARCINOGENESIS, V34, P2061, DOI 10.1093/carcin/bgt154
  41. Rutkowska E, 2013, ACTA POL PHARM, V70, P3
  42. Simonyi A, 2010, MOL NEUROBIOL, V41, P73, DOI 10.1007/s12035-010-8107-7
  43. Stefanska J, 2008, MEDIAT INFLAMM, DOI 10.1155/2008/106507
  44. Takac I, 2012, CURR HYPERTENS REP, V14, P70, DOI 10.1007/s11906-011-0238-3
  45. Tan AS, 2000, J IMMUNOL METHODS, V238, P59, DOI 10.1016/S0022-1759(00)00156-3
  46. Winterbourn C. C., 2014, BIOCHIM BIOPHYS ACTA, V1840, P730
  47. Ximenes VF, 2005, BRAZ J MED BIOL RES, V38, P1575, DOI 10.1590/S0100-879X2005001100003
  48. Zeraik ML, 2012, CURR MED CHEM, V19, P5405
  49. Zhou H, 2012, FREE RADICAL BIO MED, V52, P303, DOI 10.1016/j.freeradbiomed.2011.10.488
  50. Zhou MJ, 1997, ANAL BIOCHEM, V253, P162, DOI 10.1006/abio.1997.2391

Coleções
Artigos e Materiais de Revistas Científicas - LIM/36