Fucoxanthin Ameliorates Oxidative Stress and Airway Inflammation in Tracheal Epithelial Cells and Asthmatic Mice.

Shu-Ju Wu,Shu-Chen Cheng,Ya-Ling Chen,Wen-Chung Huang,Chian-Jiun Liou

doi:10.3390/cells10061311

Abstract

Fucoxanthin is isolated from brown algae and was previously reported to have multiple pharmacological effects, including anti-tumor and anti-obesity effects in mice. Fucoxanthin also decreases the levels of inflammatory cytokines in the bronchoalveolar lavage fluid (BALF) of asthmatic mice. The purpose of the present study was to investigate the effects of fucoxanthin on the oxidative and inflammatory responses in inflammatory human tracheal epithelial BEAS-2B cells and attenuated airway hyperresponsiveness (AHR), airway inflammation, and oxidative stress in asthmatic mice. Fucoxanthin significantly decreased monocyte cell adherence to BEAS-2B cells. In addition, fucoxanthin inhibited the production of pro-inflammatory cytokines, eotaxin, and reactive oxygen species in BEAS-2B cells. Ovalbumin (OVA)-sensitized mice were treated by intraperitoneal injections of fucoxanthin (10 mg/kg or 30 mg/kg), which significantly alleviated AHR, goblet cell hyperplasia and eosinophil infiltration in the lungs, and decreased Th2 cytokine production in the BALF. Furthermore, fucoxanthin significantly increased glutathione and superoxide dismutase levels and reduced malondialdehyde (MDA) levels in the lungs of asthmatic mice. These data demonstrate that fucoxanthin attenuates inflammation and oxidative stress in inflammatory tracheal epithelial cells and improves the pathological changes related to asthma in mice. Thus, fucoxanthin has therapeutic potential for improving asthma.

Highlights

Bronchial asthma is one of the most common respiratory allergies and inflammatory diseases globally
In the BEAS-2B cells, fucoxanthin significantly decreased the levels of CCL5, CCL11, CCL24, IL-6, IL-8, and MCP-1 compared to the TNF-α/IL-4-stimulated BEAS-2B cells (Figure 1B–G)
Under the protection of fucoxanthin treatment, we found that TNF-α/IL-4-stimulation in BEAS-2B cells reduced the release of IL-8, MCP-1, and CCL5, which would contribute to a reduction in macrophage and neutrophil infiltration of the lungs as well as inflammation and oxidative damage in the lung tissue

Summary

Introduction

Bronchial asthma is one of the most common respiratory allergies and inflammatory diseases globally. Severe air pollution produces more suspended particles and chemical irritants and increases the prevalence of asthma and respiratory disease in developing and developed countries [1]. Many studies have pointed out that the airways of patients with chronic asthma are excessively sensitive to allergens, chemical irritants, and particle pollution. Other studies have confirmed that mites, cigarette smoke, pollen, cold air, and ozone may stimulate sudden allergic reactions in the airways and asthma attacks [3]. Allergic stimulants induce hyperplasia and sensitivity of the tracheal epithelial cells. These tracheal epithelial cells increase mucus secretion, leading to airway obstruction, breathing difficulties, and even suffocation [4]

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