Polyphenon-60 displays a therapeutic effect on acne by suppression of TLR2 and IL-8 expression via down-regulating the ERK1/2 pathway
- Authors
- Jung, Min Kyung; Ha, Soogyeong; Son, Ju-ah; Song, Ji Hye; Houh, Younkyung; Cho, Eujin; Chun, Ji Hoon; Yoon, Suk Ran; Yang, Yoolhee; Bang, Sa Ik; Kim, Minjung; Park, Hyun Jeong; Cho, Daeho
- Issue Date
- Oct-2012
- Publisher
- SPRINGER
- Keywords
- Acne therapy; Polyphenon-60; Toll like receptor 2; Interleukin-8; Extracellular signal-regulated kinases 1/2; Activator protein-1
- Citation
- ARCHIVES OF DERMATOLOGICAL RESEARCH, v.304, no.8, pp 655 - 663
- Pages
- 9
- Journal Title
- ARCHIVES OF DERMATOLOGICAL RESEARCH
- Volume
- 304
- Number
- 8
- Start Page
- 655
- End Page
- 663
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/11831
- DOI
- 10.1007/s00403-012-1249-x
- ISSN
- 0340-3696
1432-069X
- Abstract
- Propionibacterium acnes (P. acnes) is a well-known 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.
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Collections - 대학 > 기초교양대학 > 기초교양학부 > 1. Journal Articles
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