Preventive Effect of Epigallocatechin Gallate, the Main Component of Green Tea, on Acute Lung Injury Caused by Air Pollutants.
Ken Ichiro TanakaShunsuke NakaguchiSachie ShiotaYuka NakadaKaho OyamaOkina SakakibaraMikako ShimodaAkio SugimotoMasaki IchitaniTakanobu TakiharaHitoshi KinugasaMasahiro KawaharaPublished in: Biomolecules (2022)
Reducing the health hazards caused by air pollution is a global challenge and is included in the Sustainable Development Goals. Air pollutants, such as PM 2.5 , induce respiratory and cardiovascular disorders by causing various inflammatory responses via oxidative stress. Catechins and polyphenols, which are components of green tea, have various protective effects, owing to their antioxidant ability. The main catechin in green tea, epigallocatechin gallate (EGCG), is potentially effective against respiratory diseases, such as idiopathic pulmonary fibrosis and asthma, but its effectiveness against air-pollution-dependent lung injury has not yet been investigated. In this study, we examined the effect of EGCG on urban aerosol-induced acute lung injury in mice. Urban aerosol treatment caused increases in inflammatory cell counts, protein levels, and inflammatory cytokine expression in the lungs of ICR mice, but pretreatment with EGCG markedly suppressed these responses. Analyses of oxidative stress revealed that urban aerosol exposure enhanced reactive oxygen species (ROS) production and the formation of ROS-activated neutrophil extracellular traps (NETs) in the lungs of mice. However, ROS production and NETs formation were markedly suppressed by pretreating the mice with EGCG. Gallocatechin gallate (GCG), a heat-epimerized form of EGCG, also markedly suppressed urban aerosol-dependent inflammatory responses and ROS production in vivo and in vitro. These findings suggest that EGCG and GCG prevent acute lung injury caused by urban aerosols through their inhibitory effects on ROS production. Thus, we believe that foods and medications containing EGCG or GCG may be candidates to prevent the onset and progression of acute lung injury caused by air pollutants.
Keyphrases
- reactive oxygen species
- oxidative stress
- air pollution
- dna damage
- lipopolysaccharide induced
- idiopathic pulmonary fibrosis
- cell death
- lps induced
- water soluble
- high fat diet induced
- diabetic rats
- particulate matter
- heavy metals
- lung function
- public health
- systematic review
- randomized controlled trial
- stem cells
- chronic obstructive pulmonary disease
- induced apoptosis
- adipose tissue
- mental health
- climate change
- high resolution
- heat stress
- mass spectrometry
- interstitial lung disease
- insulin resistance
- bone marrow
- systemic sclerosis
- small molecule
- amino acid
- high glucose
- peripheral blood
- atomic force microscopy
- global health