Vincamine prevents lipopolysaccharide induced inflammation and oxidative stress via thioredoxin reductase activation in human corneal epithelial cells.

摘要: Lipopolysaccharide (LPS) induced keratitis is a progressive infectious ocular disease in which innate inflammatory responses often cause clinical tissue damage and vision loss. In this study, the potential protective effects of vincamine, plant alkaloid used clinically as peripheral vasodilator, against LPS inflammation oxidative stress were investigated on human corneal epithelial cells (HCECs). HCECs treated with vincamine at various concentrations. Cell viability, reactive oxygen species (ROS) levels, gene expression levels interleukin-6 (IL-6), IL-8, IL-1β, TNF-α, transforming growth factor-β (TGF-β) HCECs, assessed. The antioxidant was evaluated by measuring malondialdehyde (MDA), total capacity (T-AOC), superoxide dismutase (SOD). intracellular activities thioredoxin reductase (TrxR) well other anti-oxidant proteins also HCECs. results showed that protected from cell viability reduction ameliorated inflammation. Vincamine exhibited strong activity, decreasing ROS regulating SOD, T-AOC MDA. exerted anti-inflammatory IL-6, TGF-β expression. Intracellular TrxR activity significantly activated vincamine. These findings suggest exerts positive may be useful protecting keratitis.