EGCG alleviates PM2.5-induced lung injury via activation of PPAR-γ to suppress inflammation and oxidative stress

作者：Kai Liu, Dean Wu, Chunyan Li, Dongxia Tang, Xu Chen, T. Li · 发表于：Frontiers in Pharmacology · 年份：2025 · DOI：10.3389/fphar.2025.1695785 · 被引用次数：2 · 研究领域：Heme Oxygenase-1 and Carbon Monoxide、Tea Polyphenols and Effects、Chronic Obstructive Pulmonary Disease (COPD) Research

Fine particulate matter (PM2.5), a prevalent air pollutant, induces pulmonary injury by triggering inflammatory responses and oxidative stress, leading to cellular damage and tissue disruption. Epigallocatechin gallate (EGCG), a natural polyphenol compound derived from plants and known for its anti-inflammatory and antioxidant properties, has not been thoroughly investigated regarding its protective role and underlying mechanisms against PM2.5 triggered lung injury. This study employed a murine model of lung injury triggered by PM2.5 and the BEAS-2B cells to evaluate the effects of EGCG. We measured the levels of inflammatory cytokines and oxidative stress markers, alongside examining the expression of peroxisome proliferator-activated receptor gamma (PPAR-γ) and its downstream effectors nuclear factor-kappa B (NF-κB) and heme oxygenase-1 (HO-1). PM2.5 exposure induced pathological alterations in mouse lung tissues, including inflammatory cell infiltration and alveolar wall thickening. Both in vivo and in vitro , PM2.5 elevated pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), increased reactive oxygen species and malondialdehyde levels, and reduced the activity of antioxidant enzymes (catalase and superoxide dismutase). Furthermore, PM2.5 suppressed PPAR-γ expression, activated NF-κB signaling, and decreased HO-1 expression. Pretreatment with EGCG effectively upregulated PPAR-γ expression, subsequently inhibited NF-κB activation, and enhanced HO-1 activity, thereby attenu...