NDLI: Epigallocatechin-3-gallate (EGCG) Suppresses the Trafficking of Lymphocytes to Epidermal Melanocytes via Inhibition of JAK2: Its Implication for Vitiligo Treatment.

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Epigallocatechin-3-gallate (EGCG) Suppresses the Trafficking of Lymphocytes to Epidermal Melanocytes via Inhibition of JAK2: Its Implication for Vitiligo Treatment.

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Epigallocatechin-3-gallate (EGCG) Suppresses the Trafficking of Lymphocytes to Epidermal Melanocytes via Inhibition of JAK2: Its Implication for Vitiligo Treatment.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ning, Weixuan Wang, Suiquan Dong, Xiaowu Liu, Dongyin Fu, Lifang Jin, Rong Xu, Aie
Description	Author Affiliation: Ning W ( Department of Dermatology, Guangxing Affiliated Hospital of Zhejiang Chinese Medical University.)
Abstract	Vitiligo is an inflammatory skin disorder in which activated T cells play an important role in its onset and progression. Epigallocatechin-3-gallate (EGCG), the major chemical constituent of green tea, exhibits remarkable anti-oxidative and anti-inflammatory properties. EGCG administration has been confirmed to decrease the risk of vitiligo; however, the underlying mechanism is undetermined. In this study, we proved that EGCG directly inhibited the kinase activity of Janus kinase 2 (JAK2). In primary cultured human melanocytes, EGCG pre-treatment attenuated interferon (IFN)-Î³-induced phosphorylation of JAK2 and its downstream signal transducer and activator of transcription (STAT)1 and STAT3 in a dose-dependent manner. We further examined the chemoattractant expression in melanocytes and demonstrated that EGCG significantly inhibited IFN-Î³-induced expression of intracellular adhesion molecule (ICAM)-1, CXCL10, and monocyte chemotactic protein (MCP)-1 in human melanocytes. In addition, EGCG reduced the protein levels of the corresponding receptors including CD11a, CXCR3, and CCR2 in human T lymphocytes. As a consequence, adhesion of human T cells to melanocytes induced by IFN-Î³ was effectively suppressed by EGCG. Taken together, our results provided new evidence for the effectiveness of EGCG in vitiligo treatment and supported JAK2 as a molecular target for vitiligo medicine development.
File Format	HTM / HTML
ISSN	09186158
e-ISSN	13475215
Journal	Biological & Pharmaceutical Bulletin
Issue Number	11
Volume Number	38
Language	English
Publisher	The Pharmaceutical Society of Japan J-STAGE
Publisher Date	2015-01-01
Publisher Place	Japan
Access Restriction	Open
Subject Keyword	Discipline Biochemistry Discipline Pharmacology Camellia Sinensis Chemistry Catechin Analogs & Derivatives Epidermis Drug Effects Janus Kinase 2 Metabolism Phytotherapy T-lymphocytes Vitiligo Drug Therapy Anti-inflammatory Agents Pharmacology Therapeutic Use Antigens, Cd11a Antioxidants Cell Movement Cytology Pathology Intercellular Adhesion Molecule-1 Interferon-gamma Melanocytes Phosphorylation Plant Extracts Receptors, Ccr2 Stat3 Transcription Factor Signal Transduction Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Medicine Pharmacology Pharmaceutical Science

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Epigallocatechin-3-gallate (EGCG) Suppresses the Trafficking of Lymphocytes to Epidermal Melanocytes via Inhibition of JAK2: Its Implication for Vitiligo Treatment.

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Epigallocatechin-3-gallate (EGCG) Suppresses the Trafficking of Lymphocytes to Epidermal Melanocytes via Inhibition of JAK2: Its Implication for Vitiligo Treatment.

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