Tea Polyphenols Selectively Inhibit Proliferation and Migration of Airway Smooth Muscle Cells

Mengmeng Yang,Huan Zhou,Yue Wang,Lei Liu,Darcy E Wagner,Defeng Xu,Fang Liang

doi:10.5296/jbls.v9i2.13018

Abstract

Airway smooth muscle cells (ASMCs) have been recommended as a target for the treatment of inflammation and narrowing of the airways in asthma. New safe and efficient approaches to relieve symptoms caused by ASMCs is highly desired. Inspired by the inhibitory effects of tea polyphenols on vascular smooth muscle cells (VSMCs), tea polyphenols were applied in the current work to evaluate their regulation of ASMCs in vitro. A dose-dependent decrease of ASMCs density was observed after 24 h incubation with tea polyphenols. Additionally, ASMCs were significantly more sensitive to tea polyphenols than human bronchial epithelial cells (HBECs). Tea polyphenol treatment led to a dose dependent inhibition on ASMC migration and reduced the gene expression of nuclear factor-κB (NF-κB). In studies which compared the four main polyphenolic constituents of tea polyphenols—including epicatechin (EC), epicatechingallate (ECG), epigallocatechin (EGC) and epigallocatechingallate (EGCG)—on the proliferation of ASMCs, EGC was identified as being the most potent. These results suggest tea polyphenols are a promising agent for ASMCs targeted asthma control.

Highlights

The acute narrowing of the airway and airflow obstruction in asthma is caused by abnormal contractions as well as mass increase of airway smooth muscle (ASM) (Solway & Irvin, 2007)
3.1 Effects of tea polyphenols on the proliferation of Airway smooth muscle cells (ASMCs) and human bronchial epithelial cells (HBECs) ASMCs exposed to tea polyphenols (Fig.1a) exhibited a dose-dependent decrease in metabolic activity after 24 h incubation as assessed by MTT (p
In contrast to the dose-dependent effects we observed in ASMCs, we observed no significant decreases in HBECs with tea polyphenol treatment, even in the presence of increasing doses (Fig.1d)

Summary

Introduction

The acute narrowing of the airway and airflow obstruction in asthma is caused by abnormal contractions as well as mass increase of airway smooth muscle (ASM) (Solway & Irvin, 2007). Several drugs targeting ASMCs have been developed over the past few decades, including β-agonists, anti-histamines and anti-leukotrienes (Siddiqui et al, 2013) While they can relieve the symptoms of dyspnea, they have limited effects on the structural alterations of the airways caused by diseased ASM. Bronchial thermoplasty is an FDA approved technology to control increased ASM mass in severe asthmatics which do not respond to conventional therapies such as inhaled corticosteroids (ICS) and long-acting β2-agonists (LABAs) (Wahidi & Kraft, 2012). It aims to reduce ASM mass in the airways via delivering controlled thermal energy through a bronchoscopically placed probe to the airway walls within a series of three bronchoscopies. Development of safe and efficient approaches to control or reduce ASM mass beyond bronchial thermoplasty is needed

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Discussion

Conclusion