Abstract
Purpose:
Inflammation and oxidative stress are principal contributors to the pathogenesis of numerous ocular conditions, including keratitis. Lipopolysaccharide (LPS)-induced corneal inflammation is a commonly used in vitro model to explore the anti-inflammatory and antioxidant potential of novel therapeutic agents.
Methods:
Human corneal epithelial cells (HCECs) were stimulated with LPS to reproduce an inflammatory microenvironment. Rosmarinic acid was administered at different concentrations, and its effects were evaluated using several endpoints. Cell viability was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Intracellular reactive oxygen species (ROS), pro-inflammatory cytokines (interleukin [IL]-6, IL-1β, tumor necrosis factor-α [TNF-α]), transforming growth factor-β (TGF-β), and nuclear factor erythroid 2-related factor 2 (Nrf2) and Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) were quantified at mRNA and protein levels.
Results:
Rosmarinic acid significantly restored cell viability, reduced ROS generation, and suppressed pro-inflammatory cytokine expression in a concentration-dependent manner. Furthermore, it modulated TGF-β expression and normalized NF-κB and Nrf2 levels suggesting a broader regulatory effect on inflammatory and repair mechanisms.
Conclusions:
These findings underscore the potent anti-inflammatory and antioxidative properties of rosmarinic acid in HCECs. Rosmarinic acid may represent a promising therapeutic avenue for the management of corneal inflammation and oxidative stress-induced ocular pathologies.
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