Vulpinic acid, a lichen metabolite, emerges as a potential drug candidate in the therapy of oxidative stress-related diseases, such as atherosclerosis

Vulpinic acid, a lichen compound, has been shown to have many beneficial effects and its medicinal value increases day by day. As in atherosclerosis, endothelial damage is the basis of many diseases. The aim of this study is to investigate the effects of vulpinic acid against oxidative stress damage induced by hydrogen peroxide (H₂O₂) in endothelial cells. In order to find the IC₅₀ of H₂O₂ and the protective dose of vulpinic acid, methyl thiazolyldiphenyl tetrazolium bromide (MTT) assays were performed. The amount of Reactive Oxygen Species (ROS) induced by H₂O₂ and the protective effects of vulpinic acid against ROS were examined by fluorometric DCF-DA kit. The effects of H₂O₂ and vulpinic acid on actin filaments were determined by tetramethyl rhodamine (TRITC)-phalloidin fluorescence staining. Expression of Tie2 proteins was immunocytochemically analyzed in H₂O₂- and vulpinic acid-treated cells. After 24 h, the IC₅₀ was found to be 215 μM in HUVECs treated with H₂O₂. The most effective dose of vulpinic acid against H₂O₂-associated damage was found to be 15 μM. Vulpinic acid pretreatment was shown to reduce H₂O₂-induced ROS production significantly ( p < 0.05). It was shown that 215 μM of H₂O₂ caused actin fragmentation, cell shrinkage, and decrease in actin florescence intensity while vulpinic acid protected the cells from these damages. It was found that Tie2 immunoreactivity was decreased in H₂O₂-treated groups and vulpinic acid pretreatment reduced the expression of this protein. In conclusion, vulpinic acid decreases H₂O₂-induced oxidative stress and oxidative stress-related damages in HUVECs. It may be drug candidate in the therapy of atherosclerosis.