Polyphenon-60 displays a therapeutic effect on acne by suppression of TLR2 and IL-8 expression via down-regulating the ERK1/2 pathway

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Title
Polyphenon-60 displays a therapeutic effect on acne by suppression of TLR2 and IL-8 expression via down-regulating the ERK1/2 pathway
Author(s)
M K Jung; S Ha; J A Son; J H Song; Y Hough; E Cho; J H Chun; Suk Ran Yoon; Y Yang; S I Bang; M Kim; H J Park; D Cho
Bibliographic Citation
Archives of Dermatological Research, vol. 304, no. 8, pp. 655-663
Publication Year
2012
Abstract
Propionibacterium acnes (P. acnes) is a wellknown acne-inducing factor which causes inflammatory skin lesions by enhancing cytokine production through toll-like receptor 2 (TLR2). Green tea extract catechin has been documented to possess anti-inflammatory effects. However, little is known about the mechanisms involved or any direct effect of green tea catechin on acne. The present study investigated the therapeutic effects and mechanism of polyphenon-60, also known as green tea catechin compound, on acne in vitro and in vivo. In a clinical study using topical polyphenon-60 treatment, acne patients showed symptomatic improvement with decrease in the number of comedos and pustules. To investigate the mechanism underlying the activity of polyphenon-60 in acne therapy, an in vitro study was performed. We found that polyphenon-60 reduced the levels of P. acnes-enhanced TLR2 and interleukin-8 (IL-8) in THP-1 cells, human monocyte cell line and human primary monocytes. Taken together, these data demonstrate that polyphenon-60 has a therapeutic effect on acne by suppressing inflammation, specifically by inhibiting TLR2 expression and IL-8 secretion via down-regulation of extracellular signal-regulated kinases 1/2 (ERK1/2) pathway and activator protein-1 (AP-1) pathway.
Keyword
Acne therapyActivator protein-1Extracellular signal-regulated kinases 1/2Interleukin-8Polyphenon-60Toll like receptor 2
ISSN
0340-3696
Publisher
Springer
DOI
http://dx.doi.org/10.1007/s00403-012-1249-x
Type
Article
Appears in Collections:
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
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