Epigallocatechin‐3‐Gallate Inhibits Collagen Production of Nasal Polyp‐Derived Fibroblasts

Abstract

Nasal polyps are chronic inflammatory conditions characterized by myofibroblast differentiation and extracelluar matrix accumulation. The major catechin from green tea is (-)-epigallocatechin-3-gallate (EGCG), which has garnered attention for its potential to prevent oxidative stress-related diseases. The purpose of this study was twofold: (i) to determine the effect of EGCG on fibroblast differentiation into myofibroblasts and extracellular matrix accumulation in transforming growth factor (TGF)-β1-induced nasal polyp-derived fibroblasts (NPDFs) and (ii) to determine if the antioxidative effect of EGCG on reactive oxygen species (ROS) production in TGF-β1-induced NPDFs is involved in the aforementioned processes. TGF-β1-induced NPDFs were treated with or without EGCG. α-smooth muscle actin (α-SMA) and collagen type I mRNA were analyzed by reverse transcription-polymerase chain reaction. α-SMA protein was also detected using immunofluorescent staining. The amount of total soluble collagen was analyzed by Sircol collagen assay. ROS activity was measured by the nitroblue tetrazolium reduction assay and visualized by fluorescent microscopy. EGCG significantly inhibited expressions of α-SMA and collagen type I mRNA and reduced α-SMA and collagen protein levels at concentrations of 10-20 µg/mL. EGCG also inhibited TGF-β1-induced ROS production at the same concentrations. These results suggest the possibility that EGCG may be effective at inhibiting the development of nasal polyps through an anti-oxidant effect.

The Polyphenols (−)-Epigallocatechin-3-Gallate and Luteolin Synergistically Inhibit TGF-β-Induced Myofibroblast Phenotypes through RhoA and ERK Inhibition

“…Our laboratory and others have found that EGCG and luteolin are capable of preventing development and/or maintenance of myofibroblast phenotypes when used at relatively high micromolar concentrations. Our most effective dose of EGCG was similar to that found by Kang et al who showed that approximately 20–40 µM EGCG inhibited α-SMA and collagen type I production in nasal polyp-derived fibroblasts [50] and to another study which found that 40 µM EGCG largely obliterated fibronectin production in primary dermal fibroblasts [51] . However, these concentrations are likely to have off-target effects, causing deleterious toxicity in vivo and likely represent concentrations that cannot be achieved in vivo .…”

Curcumin analog A13 alleviates oxidative stress by activating Nrf2/ARE pathway and ameliorates fibrosis in the myocardium of high-fat-diet and streptozotocin-induced diabetic rats

“…Studies have shown that TGF-β1 promotes mRNA expression of type I collagen in fibroblasts [19,20], stimulates the proliferation of cardiac fibroblasts and collagen synthesis [21]. Myocardial fibrosis is characterized by myocardial stromal remodeling; hyperglycemia, oxidative stress and excessive accumulation of ROS may be important factors in the formation and development of myocardial fibrosis [22,23].…”

Inhibitory effect of maple syrup on the cell growth and invasion of human colorectal cancer cells

“…These data suggest that maple syrup might affect the expression or activation of enzymes, such as MMP-2 and MMP-9, which play an important role in cell invasion of the extracellular matrix, including the basement membrane. Although there is no report on the effect of maple syrup on cell invasion, a recent study reported that polyphenols such as epigallocatechin-3-gallate inhibit MMP-2 and MMP-9 expression ( 24 – 28 ). Therefore, the expression levels of MMP-2 and MMP-9 in CRC cells might be inhibited by polyphenols such as quebecol and ginnalins that are present in maple syrup.…”