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

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