Journal of the Society of Cosmetic Scientists of Korea (대한화장품학회지)

Society of Cosmetic Scientists of Korea (대한화장품학회)
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Fractionated Trapa japonica Extracts Inhibit ROS-induced Skin Inflammation in HaCaT keratinocytes

각질형성세포에서 ROS로 유도된 염증반응에 대한 능실 추출물 및 그 분획물의 항염 효과

  • Received : 2014.12.15
  • Accepted : 2015.03.12
  • Published : 2015.03.31
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Abstract

Ultraviolet B (UVB) irradiation induces both production of reactive oxygen species (ROS) and glucocorticoids (GCs)-mediated stress responses such as an increase of $11{\beta}$-hydroxysteroid dehydrogenase type 1 ($11{\beta}$-HSD1) activity in skin. In addition, ROS-induced inflammatory mediators and proinflammatory cytokines trigger skin inflammation. In this study, as $11{\beta}$-HSD1 inhibitor recovered a decrease of catalase expression, we investigated whether Trapa japonica (TJ) extract and its fractions could inhibit $11{\beta}$-HSD1/ROS-induced skin inflammation in HaCaT keratinocytes. TJ extract and its fractions inhibited expressions of $11{\beta}$-HSD1 as well as the increase of ROS in UVB-exposed HaCaT keratinocytes. Moreover, proinflammatory cytokines such as interleukin (IL)- ${\alpha}$, - ${\beta}$ and tumor necrosis factor (TNF)-${\alpha}$, and cyclooxygenase (COX)-2 and inducible NO synthase (iNOS) as inflammatory mediators were also inhibited in both mRNA and protein levels. Finally, prostaglandin $E_2$ ($PGE_2$) produced by COX-2 was inhibited effectively by TJ extract and its fractions. Taken together, these results suggest that TJ extract could be a potential anti-inflammatory ingredient to inhibit UVB-induced inflammation in skin.

자외선은 외부적인 스트레스 자극인자로 작용하여 사람 각질형성세포에서 reactive oxygen species (ROS)와 비활성 코르티손을 활성 코르티솔로 전환시키는 효소인 $11{\beta}$-hydroxysteroid dehydrogenase type 1 ($11{\beta}$-HSD1)의 발현 및 활성을 증가시킨다고 알려져 있다. 또한, ROS가 증가된 피부에서는 염증 유발 사이토카인과 염증 매개 인자의 발현이 증가되어 결과적으로 염증반응을 일으키게 되는 원인이 된다. 본 연구에서는 각질형성세포(HaCaT)에서 $11{\beta}$-HSD1 억제제가 ROS 분해효소인 catalase의 생성을 회복시킴에 착안하여, $11{\beta}$-HSD1의 발현을 저해함과 동시에 ROS로부터 유도되는 염증 반응을 억제하는 천연물 소재를 발굴하고자 하였다. 그 중 능실 추출물과 그 분획물은 각각 $11{\beta}$-HSD1의 발현과 ROS 생성 증가를 억제하고, 염증성 사이토카인인 tumor necrosis factor (TNF)-${\alpha}$, interleukin (IL)-$1{\alpha}$, $-1{\beta}$의 발현을 억제하였다. 또한, 자외선에 의해 유도되는 염증 매개인자인 cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS), prostaglandin $E_2$ ($PGE_2$)의 생성을 저해하였다. 따라서 본 연구 결과로부터 능실 추출물 및 그 분획물은 $11{\beta}$-HSD1의 발현을 억제함과 동시에 ROS에 의해 유발된 피부 염증 반응을 효과적으로 저해함을 확인하였다.

Keywords

References

  1. D. C. Lebert and A. Huttenlocher, Inflammation and wound repair, Semin. Immunol., 26(4), 315 (2014).
  2. A. Amaro-Ortiz, B. Yan, and J. A. D'Orazio, Ultraviolet radiation, aging and the skin: Prevention of damage by topical cAMP manipulation, Molecules, 19(5), 6202 (2014). https://doi.org/10.3390/molecules19056202
  3. H.-Y. Thong and H. I. Maibach, Irritant dermatitisas a model of inflammation, Drug Discov. Today: Disease Mechanisms, 5(2), 221 (2008). https://doi.org/10.1016/j.ddmec.2008.02.002
  4. Y. Matsumura and H. N. Ananthaswamy, Toxic effects of ultraviolet radiation on the skin, Toxicol. Appl. Pharmacol., 195(3), 298 (2004). https://doi.org/10.1016/j.taap.2003.08.019
  5. A. Takashima and P. R. Bergstresser, Impact of UVB radiation on the epidermal cytokine network, Photochem. Photobiol., 63(4), 397 (1996). https://doi.org/10.1111/j.1751-1097.1996.tb03054.x
  6. A. Pupe, R. Moison, P. D. Haes, G. Beijersbergen van Henegouwen, L. Rhodes, H. Degreef, and M. Garmyn, Eicosapentaenoic acid, a n-3 polyunsaturated fatty acid differentially modulates TNF-${\alpha}$, IL-1${\alpha}$, IL-6 and PGE2 expression in UVB-irradiated human keratinocytes, J. Invest. Dermatol., 118(4), 692 (2002). https://doi.org/10.1046/j.1523-1747.2002.01615.x
  7. B. Nedoszytko, M. Sokolowska-Wojdylo, K. Ruckemann-Dziurdzinska, J. Roszkiewicz, and R. J. Nowicki, Chemokines and cytokines network in the pathogenesis of the inflammatory skin diseases: atopic dermatitis, psoriasis and skin mastocytosis, Postepy. Dermatol. Alergol., 31(2), 84 (2014).
  8. I. Striz, E. Brabcova, L. Kolesar, and A. Sekerkova. Cytokine networking of innate immunity cells: a potential target of therapy, Clin. Sci. (Lond)., 126(9), 593 (2014). https://doi.org/10.1042/CS20130497
  9. F. Giuliano and T. D. Warner, Origins of prostaglandin E2: involvements of cyclooxygenase (COX)-1 and COX-2 in human and rat systems, J Pharmacol. Exp. Ther., 303(3), 1001 (2002). https://doi.org/10.1124/jpet.102.041244
  10. M. Schafer and S. Werner, Oxidative stress in normal and impaired wound repair, Pharmacol. Res., 58(2), 165 (2008). https://doi.org/10.1016/j.phrs.2008.06.004
  11. C. H. Hong, S. K. Hur, O. J. Oh, S. S. Kim, K. A. Nam, and S. K. Lee. Evaluation of natural products on inhibition of inducible cyclooxygenase (COX-2) and nitric oxide synthase (iNOS) in cultured mouse macrophage cells, J. Ethnopharmacol., 83(1-2), 153 (2002). https://doi.org/10.1016/S0378-8741(02)00205-2
  12. Y. H. Jean, W. F. Chen, C. Y. Duh, S. Y. Huang, C. H. Hsu, C. S. Lin, C. S. Sung, I. M. Chen, and Z. H. Wen, Inducible nitric oxide synthase and cyclooxygenase- 2 participate in anti-inflammatory and analgesic effects of the natural marine compound lemnalol from Formosan soft coral Lemnalia cervicorni, Eur. J. Pharmacol., 578(2-3), 323(2008). https://doi.org/10.1016/j.ejphar.2007.08.048
  13. G. Rhie, M. H. Shin, J. Y. Seo, W. W. Choi, K. H. Cho, K. H. Kim, K. C. Park, H. C. Eun, and J. H. Chung, Aging- and photoaging-dependent changes of enzymic and noenzyme antioxidants in the epidermis and dermis of human skin in vivo, J. Invest. Dermatol., 117(5), 1212 (2001). https://doi.org/10.1046/j.0022-202x.2001.01469.x
  14. M. M. Suter, K. Schulze, W. Bergman, M. Welle, P. Roosje, and E. J. Muller, The keratinocyte in epidermal renewal and defence, Vet. Dermatol., 20(5-6), 515 (2009). https://doi.org/10.1111/j.1365-3164.2009.00819.x
  15. T. Bito and C. Nishigori, Impact of reactive oxygen species on keratinocyte signaling pathways, J. Dermatol. Sci., 68(1), 3 (2012). https://doi.org/10.1016/j.jdermsci.2012.06.006
  16. H. Masaki, Role of antioxidants in the skin: Anti-aging effects, J. Dermatol. Sci., 58(2), 85 (2010). https://doi.org/10.1016/j.jdermsci.2010.03.003
  17. R. T. Narendhirakannan and M. A. Hannah, Oxidative stress and skin cancer: an overview, Indian J. Clin. Biochem., 28(2), 110 (2013). https://doi.org/10.1007/s12291-012-0278-8
  18. M. Wamil and J. R. Seckl, Inhibition of 11beta-hydroxysteroid dehydrogenase type 1 as a promising therapeutic target, Drug Discov. Today, 12(13-14), 504 (2007). https://doi.org/10.1016/j.drudis.2007.06.001
  19. J. S. Scott, F. W. Goldberg, and A. V. Turnbull, Medicinal chemistry of inhibitors of $11\beta$-hydroxysteroid dehydrogenase type 1 ($11{\beta}$-HSD1), J. Med. Chem., 57(11), 4466 (2014). https://doi.org/10.1021/jm4014746
  20. S. Itoi, M. Terao, H. Murota, and I. Katayama, $11{\beta}$ -Hydroxysteroid dehydrogenase 1 contributes to the pro-inflammatory response of keratinocytes, Biochem. Biophys. Res. Commun., 440(2), 265 (2013). https://doi.org/10.1016/j.bbrc.2013.09.065
  21. M. Terao, H. Murota, A. Kimura, A. Kato, A. Ishikawa, K. Igawa, E. Miyoshi, and I. Katayama, $11{\beta}$-hydroxysteroid dehydrogenase-1 is a novel regulator of skin homeostasis and a candidate target for promoting tissue repair, PLoS ONE, 6(9), e25039 (2011). https://doi.org/10.1371/journal.pone.0025039
  22. A. Tiganescu, E. A. Walker, R. S. Hardy, A. E. Mayes, and P. M. Stewart, Localization, age- and site-dependent expression, 11beta-hydroxysteroid dehydrogenase type 1 in skin, J. Invest. Dermatol., 131(1), 30 (2011). https://doi.org/10.1038/jid.2010.257
  23. A. Tiganescu, A. A. Tahrani, S. A. Morgan, M. Otranto, A. Desmouliere, L. Abrahams, Z. Hassan-Smith, E. A. Walker, E. H. Rabbit, M. S. Cooper, K. Amrein, G. G. Lavery, and P. M. Stewart, $11{\beta}$-Hydroxysteroid dehydrogenase blockade prevents age-induced skin structure and function defects, J. Clin. Invest., 123(7), 3051 (2013). https://doi.org/10.1172/JCI64162
  24. C. Skobowiat, R. M. Sayre, J. C. Dowdy, and A. T. Slominski, Ultraviolet radiation regulates cortisol activity in a waveband-dependent manner in human skin ex vivo, Br. J. Dermatol., 168(3), 595 (2013). https://doi.org/10.1111/bjd.12096
  25. M. Schieber and N. S. Chandel, ROS function in redox signaling and oxidative stress, Current biol., 24(10), 453 (2014). https://doi.org/10.1016/j.cub.2014.03.034
  26. G. E. Rhie, J. Y. Seo, and J. H. Chung, Modulation of catalase in human skin in vivo by acute and chronic UV radiation, Mol. Cells, 11(3), 399 (2001).
  27. J. W. Cha, M. J. Piao, K. C. Kim, C. W. Yao, J. Zheng, S. M. Kim, C. L. Hyun, Y. S. Ahn, and J. W. Hyun, The Polyphenol Chlorogenic Acid Attenuates UVB-mediated Oxidative Stress in Human HaCaT Keratinocytes, Biomol. Ther. 22(2), 136 (2014). https://doi.org/10.4062/biomolther.2014.006
  28. U. Wolfle, P. R. Esser, B. Simon-Haarhaus, S. F. Martin, J. Lademann, and C. M. Schempp, UVB-induced DNA damage, generation of reactive oxygen species, and inflammation are effectively attenuated by the flavonoid luteolin in vitro and in vivo, Free Radic. Biol. Med., 50(9), 1081 (2011). https://doi.org/10.1016/j.freeradbiomed.2011.01.027
  29. R. E. Maldve, Y. Kim, S. J. Muga, and S. M. Fischer, Prostaglandin E(2) regulation of cyclooxygenase expression in keratinocytes is mediated via cyclic nucleotide-linked prostaglandin receptors, J. Lipid. Res., 41(6), 873 (2000).