Potential therapeutic properties of Sorbus commixta twig ethanol extract on vitiligo in skin cells


  • Da Won Jung Department of Beauty and Cosmetic Science, Eulji University, Seongnam, Gyeonggi-do, Republic of Korea https://orcid.org/0000-0002-2511-646X
  • Su Jin Lim Department of Beauty and Cosmetic Science, Eulji University, Seongnam, Gyeonggi-do, Republic of Korea https://orcid.org/0000-0003-1258-8086
  • Chang Seok Lee Department of Beauty and Cosmetic Science, Eulji University, Seongnam, Gyeonggi-do, Republic of Korea




anti-inflammation, anti-oxidative effect, melanin synthesis, Sorbus commixta twig ethanol (STE) extract, vitiligo


Paper description:

  • Pre-We started this study to demonstrate the therapeutic properties of Sorbus commixta twig ethanol extract (STE) on vitiligo.
  • Cell viability and melanin contents in STE-treated melanocytes were examined. Interleukin (IL)-6, -8 and tumor necrosis factor (TNF)-a expression were observed in dermal fibroblasts and keratinocytes by real-time PCR and ELISA.
  • STE induced cell proliferation and melanin synthesis in melanocytes. STE inhibited IL-6, IL-8 and TNF-a expression in TNF-a-stimulated fibroblasts and keratinocytes.
  • STE ameliorates vitiligo symptoms through melanin synthesis, antiinflammatory and antioxidative effects.

Abstract: Sorbus commixta is a tree of the Rosaceae family growing in Asia that has long been used to treat asthma and neuralgia. In a previous report, the chemical isolated from the bark of S. commixta was shown to suppress the production of nitric oxide (NO) and preinflammation by downregulating the NF-кB pathway in lipopolysaccharide (LPS)-induced RAW 264.7 cells. Vitiligo is an acquired immune disease, usually characterized by white spots on the skin; however, its exact cause has not been identified. This study assessed the effects of an ethanol extract of S. commixta twigs (STE) on melanocyte activation, as well as its antiinflammatory and antioxidant properties. STE significantly increased the proliferation and melanin content of B16 melanocytes. Because of the importance of tumor necrosis factor (TNF)-α in inflammatory diseases, including the stimulation of vitiligo, the antiinflammatory effects of STE were tested in TNF-α-stimulated dermal fibroblasts and keratinocytes. STE reduced the levels of expression of IL-6, IL-8 and TNF-α mRNA and proteins. To assess the underlying molecular mechanism, the effects of STE on the mitogen-activated protein kinase (MAPK) signaling process were analyzed in dermal fibroblasts. Results show that STE inactivated extracellular signal-regulated kinase (ERK). In addition, STE exhibited antioxidative properties in assays of DPPH radical scavenging activity. Taken together, these findings suggest that STE has potential therapeutic activity in vitiligo.


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Yu T, Lee YJ, Jang H-J, Kim AR, Hong S, Kim TW, Kim M-Y, Lee J, Lee YG, Cho JY. Anti-inflammatory activity of Sorbus commixta water extract and its molecular inhibitory mechanism. J Ethnopharmacol. 2011;134(2):493-500.


Taïeb A, Picardo M. The definition and assessment of vitiligo: a consensus report of the vitiligo european task force. Pigment Cell Res. 2007;20(1):27-35.


Alikhan A, Felsten LM, Daly M, Petronic-Rosic V. Vitiligo: A comprehensive overview. J Am Acad Dermatol. 2011;65(3):473-91.


Allam M, Riad H. Concise review of recent studies in vitiligo. Qatar Med J. 2014;2013(2):1-19.


Boniface K, Seneschal J, Picardo M, Taïeb A. Vitiligo: Focus on clinical aspects, immunopathogenesis, and therapy. Clin Rev Allergy Immunol. 2017;54(1):52-67.


Kundu RV, Mhlaba JM, Rangel SM, Poole ICL. The convergence theory for vitiligo: A reappraisal. Exp Dermatol. 2018;28(6):647-55.


Choi H, Kim K, Han J, Choi H, Jin SH, Lee EK, Shin DW, Lee TR, Lee A-Y, Noh M. Kojic acid-induced IL-6 production in human keratinocytes plays a role in its anti-melanogenic activity in skin. J Dermatol Sci. 2012;66(3):207-15.


Manga P, Elbuluk N, Orlow SJ. Recent advances in understanding vitiligo. F1000Research. 2016;5:2234.


Laddha NC, Dwivedi M, Begum R. Increased tumor necrosis factor (TNF)-α and its promoter polymorphisms correlate with disease progression and higher susceptibility towards vitiligo. PLoS One. 2012;7(12):e52298.


Sabio G, Davis RJ. TNF and MAP kinase signalling pathways. Semin Immunol. 2014;26(3):237-45.


Rashighi M, Harris JE. Vitiligo pathogenesis and emerging treatments. Dermatol Clin. 2017;35(2):257-65.


Xuan SH, Park YM, Park SH, Jeong HJ, Park SN. Suppression of ultraviolet B-mediated matrix metalloproteinase generation by Sorbus commixta twig extract in human dermal fibroblasts. Photochem Photobiol. 2018;94(2):370-7.


Salducci M, André N, Guéré C, Martin M, Fitoussi R, Vié K, Cario-André M. Factors secreted by irradiated aged fibroblasts induce solar lentigo in pigmented reconstructed epidermis. Pigment Cell Res. 2014;27(3):502-4.


Felsten LM, Alikhan A, Petronic-Rosic V. Vitiligo: A comprehensive overview. J Am Acad Dermatol. 2011;65(3):493-514.


Jian D, Jiang D, Su J, Chen W, Hu X, Kuang Y, Xie H, Li J, Chen X. Diethylstilbestrol enhances melanogenesis via cAMP-PKA-mediating up-regulation of tyrosinase and MITF in mouse B16 melanoma cells. Steroids. 2011;76(12):1297-304.


Dumitru CD, Ceci JD, Tsatsanis C, Kontoyiannis D, Stamatakis K, Lin J-H, Patriotis C, Jenkins NA, Copeland NG, Kollias G, Tsichlis PN. TNF-α Induction by LPS is regulated post transcriptionally via a Tpl2/ERK-Dependent Pathway. Cell. 2000;103(7):1071-83.


Schett G, Tohidast-Akrad M, Smolen JS, Schmid BJ, Steiner C-W, Bitzan P, Zenz P, Redlich K, Xu Q, Steiner G. Activation, differential localization, and regulation of the stress-activated protein kinases, extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38 mitogen-activated protein kinase, in synovial tissue and cells in rheumatoid arthritis. Arthritis Rheum. 2000;43(11):2501-12.


Trotta R, Kanakaraj P, Perussia B. Fc gamma R-dependent mitogen-activated protein kinase activation in leukocytes: a common signal transduction event necessary for expression of TNF-alpha and early activation genes. J Exp Med. 1996;184(3):1027-35.


Oeckinghaus A, Ghosh S. The NF- B Family of transcription factors and its regulation. Cold Spring Harb Perspect Biol. 2009;1(4):a000034.


Moynagh PN. The NF-κB pathway. J Cell Sci. 2005;118(20):4589-92.


Wan J, Lin F, Zhang W, Xu A, Degiorgis J, Lu H, et al. Novel approaches to vitiligo treatment via modulation of mTOR and NF-κB pathways in human skin melanocytes. Int J Biol Sci. 2017;13(3):391-400.


Xie H, Zhou F, Liu L, Zhu G, Li Q, Li C, Gao T. Vitiligo: How do oxidative stress-induced autoantigens trigger autoimmunity? J Dermatol Sci. 2016;81(1):3-9.


Bickers DR, Athar M. Oxidative stress in the pathogenesis of skin disease. J Invest Dermatol. 2006;126(12):2565-75.


Yang G, An H-J. β-sitosteryl-3-O-β-glucopyranoside isolated from the bark of Sorbus commixta ameliorates pro-inflammatory mediators in RAW 264.7 macrophages. Immunopharmacol Immunotoxicol. 2013;36(1):70-7.


Kim CS, Oh J, Subedi L, Kim SY, Choi SU, Lee KR. Two new phenolic glycosides from Sorbus commixta. Chem Pharm Bull. 2018;66(8):839-42.





How to Cite

Jung DW, Lim SJ, Lee CS. Potential therapeutic properties of Sorbus commixta twig ethanol extract on vitiligo in skin cells. Arch Biol Sci [Internet]. 2021Dec.15 [cited 2024Apr.22];73(4):483-90. Available from: https://serbiosoc.org.rs/arch/index.php/abs/article/view/7025