Inhibitory effects of epigallocatechin gallate on compound 48/80-inducedmast cell activation and passive cutaneous anaphylaxis

Li, Guang Zhao; Chai, Ok Hee; Song, Chang Ho

doi:10.1038/emm.2005.39

Cited by 14 publications

(6 citation statements)

References 31 publications

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“…GTE and its major polyphenolic components have long been reported to possess various pharmacological activities with a broad variety of health benefits (Yang et al, 2002). Recent studies have shown that some components of green tea can inhibit MC activation (Yamamoto et al, 1998;Li et al, 2005), and affect ECM metabolism/remodeling in several experimental models (Zhong et al, 2003;Kapoor et al, 2004;Nakamuta et al, 2005). In this study, we reported that GTE and EGCG had strong inhibitory effects on MC-stimulated type I collagen production in keloid fibroblasts (Figure 4).…”

Section: Discussionmentioning

confidence: 99%

“…GTE and EGCG suppressed HMC-1-stimulated type I collagen expression in keloid fibroblasts by interfering with PI-3K/Ak signaling pathway Previous studies have shown that green tea and its major catechins not only have inhibitory effects on MC activation (Li et al, 2005), but also possess antifibrogenic activity in some animal models (Nakamuta et al, 2005). To explore whether green tea extract (GTE) and (À)-epigallocatechin-3gallate (EGCG) had any effects on MC-stimulated type I collagen expression, keloid fibroblasts were pretreated with different concentrations of GTE or EGCG for 1 hour followed by co-culture with the same cell density of HMC-1 cells for additional 24 hours under normal culturing conditions.…”

Section: Mcs Stimulate Type I Collagen Expression In Keloid Fibroblasts Through Activation Pi-3k/akt and P38 Mapk Signaling Pathwaysmentioning

confidence: 99%

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Green Tea Extract and (−)-Epigallocatechin-3-Gallate Inhibit Mast Cell-Stimulated Type I Collagen Expression in Keloid Fibroblasts via Blocking PI-3K/Akt Signaling Pathways

Zhang

Kelly

Wang

et al. 2006

Journal of Investigative Dermatology

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Keloid, a chronic fibro-proliferative disease, exhibits distinctive histological features characterized by an abundant extracellular matrix stroma, a local infiltration of inflammatory cells including mast cells (MCs), and a milieu of enriched cytokines. Previous studies have demonstrated that co-culture with MCs stimulate type I collagen synthesis in fibroblasts, but the signaling mechanisms remain largely unknown. In this study, we investigated the signaling pathways involved in MC-stimulated type I collagen synthesis and the effects of green tea extract (GTE) and its major catechin, (-)-epigallocatechin-3-gallate (EGCG), on collagen homeostasis in keloid fibroblasts. Our results showed that MCs significantly stimulated type I collagen expression in keloid fibroblasts, and the upregulation of type I collagen was significantly attenuated by blockade of phosphatidylinositol-3-kinase (PI-3K), mammalian target of rapamycin (mTOR), and p38 MAPK signaling pathways, but not by blockade of ERK1/2 pathway. Furthermore, GTE and EGCG dramatically inhibited type I collagen production possibly by interfering with the PI-3K/Akt/mTOR signaling pathway. Our findings suggest that interaction between MCs and keloid fibroblasts may contribute to excessive collagen accumulation in keloids and imply a therapeutic potential of green tea for the intervention and prevention of keloids and other fibrotic diseases.

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Section: Discussionmentioning

confidence: 99%

Section: Mcs Stimulate Type I Collagen Expression In Keloid Fibroblasts Through Activation Pi-3k/akt and P38 Mapk Signaling Pathwaysmentioning

confidence: 99%

Green Tea Extract and (−)-Epigallocatechin-3-Gallate Inhibit Mast Cell-Stimulated Type I Collagen Expression in Keloid Fibroblasts via Blocking PI-3K/Akt Signaling Pathways

Zhang

Kelly

Wang

et al. 2006

Journal of Investigative Dermatology

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“…It significantly inhibited the release of compound 48/80‐induced degranulation of histamine in rat peritoneal mast cells (RPMCs). EGCG also suppressed compound 48/80‐induced PCA reaction in rats (Li et al ., ). EGCG also inhibited antigen‐induced degranulation and LTC 4 secretion in RBL‐2H3 cells across a concentration range of 10–100 μM and has been shown to block store‐operated Ca 2+ entry of this cell line, which is the main route of calcium influx in mast cells that leads to the degranulation of allergic mediators (Inoue et al ., ).…”

Section: Sources Of Mast Cell Stabilizersmentioning

confidence: 97%

Twenty‐first century mast cell stabilizers

Finn

Walsh

2013

British J Pharmacology

116

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Mast cell stabilizing drugs inhibit the release of allergic mediators from mast cells and are used clinically to prevent allergic reactions to common allergens. Despite the relative success of the most commonly prescribed mast cell stabilizer, disodium cromoglycate, in use for the preventative treatment of bronchial asthma, allergic conjunctivitis and vernal keratoconjunctivitis, there still remains an urgent need to design new substances that are less expensive and require less frequent dosing schedules. In this regard, recent developments towards the discovery of the next generation of mast cell stabilizing drugs has included studies on substances isolated from natural sources, biological, newly synthesized compounds and drugs licensed for other indications. The diversity of natural products evaluated range from simple phenols, alkaloids, terpenes to simple amino acids. While in some cases their precise mode of action remains unknown it has nevertheless sparked interest in the development of synthetic derivatives with improved pharmacological properties. Within the purely synthetic class of inhibitors, particular attention has been devoted to the inhibition of important signalling molecules including spleen TK and JAK3. The statin class of cholesterol-lowering drugs as well as nilotinib, a TK inhibitor, are just some examples of clinically used drugs that have been evaluated for their anti-allergic properties. Here, we examine each approach under investigation, summarize the test data generated and offer suggestions for further preclinical evaluation before their therapeutic potential can be realized.

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“…Complex flavonoids, such as the green tea constituent epigallocatechin gallate (EGCG), and silymarin, a mixture of flavanolignans from milk thistle (Silybum marianum), have demonstrated antiallergic activity in both in vitro and in in vivo models (Li et al, 2005;Inoue et al, 2010;Choi & Yan 2009b).…”

Section: Flavonoid Derivativesmentioning

confidence: 97%