Journal of pharmacopuncture · 2026
Acorus gramineus Solander Preserves Corneal Epithelial Barrier Integrity against PM2.5-Induced EMT-Like Remodeling via Suppression of TGF-β/Smad Signaling.
СтатьяНазвание и аннотация: Перевод в очереди
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Kim Min Yeong, Hong Su Hyun, Choi Yung Hyun
Аннотация
OBJECTIVES: To evaluate the effects of particulate matter ≤ 2.5 µm (PM2.5) on corneal epithelial barrier integrity and to examine the protective potential of Acorus gramineus Solander root extract (AGS).
METHODS: Human corneal epithelial cells (hCECs) were cultured as three-dimensional spheroids and exposed to PM2.5 with or without AGS treatment. Barrier function, tight junction (TJ) integrity, epithelial-mesenchymal transition (EMT)-related markers, inflammatory mediators, and transforming growth factor (TGF)-β/Smad signaling were analyzed.
RESULTS: PM2.5 induced structural instability of hCEC spheroids without substantial cytotoxicity, accompanied by decreased transepithelial electrical resistance and disruption of TJ proteins such as zonula occludens (ZO)-1, ZO-3, and occludin. These alterations coincided with EMT-like remodeling, characterized by the upregulation of N-cadherin and vimentin, increased expression of matrix metalloproteinases, and elevated production of inflammatory cytokines. These effects were associated with the TGF-β/Smad signaling pathway activation. AGS restored barrier integrity, suppressed EMT-like remodeling and inflammation, and inhibited TGF-β/Smad pathway activation.
CONCLUSION: PM2.5 impairs corneal epithelial barrier function through EMT-related and inflammatory mechanisms. AGS exerts protective effects by preserving TJ integrity and suppressing TGF-β/Smad signaling, suggesting its therapeutic potential against air pollution-induced ocular surface damage.
METHODS: Human corneal epithelial cells (hCECs) were cultured as three-dimensional spheroids and exposed to PM2.5 with or without AGS treatment. Barrier function, tight junction (TJ) integrity, epithelial-mesenchymal transition (EMT)-related markers, inflammatory mediators, and transforming growth factor (TGF)-β/Smad signaling were analyzed.
RESULTS: PM2.5 induced structural instability of hCEC spheroids without substantial cytotoxicity, accompanied by decreased transepithelial electrical resistance and disruption of TJ proteins such as zonula occludens (ZO)-1, ZO-3, and occludin. These alterations coincided with EMT-like remodeling, characterized by the upregulation of N-cadherin and vimentin, increased expression of matrix metalloproteinases, and elevated production of inflammatory cytokines. These effects were associated with the TGF-β/Smad signaling pathway activation. AGS restored barrier integrity, suppressed EMT-like remodeling and inflammation, and inhibited TGF-β/Smad pathway activation.
CONCLUSION: PM2.5 impairs corneal epithelial barrier function through EMT-related and inflammatory mechanisms. AGS exerts protective effects by preserving TJ integrity and suppressing TGF-β/Smad signaling, suggesting its therapeutic potential against air pollution-induced ocular surface damage.