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 (HO) in endothelial cells. In order to find the IC of HO and the protective dose of vulpinic acid, methyl thiazolyldiphenyl tetrazolium bromide (MTT) assays were performed. The amount of reactive oxygen species (ROS) induced by HO and the protective effects of vulpinic acid against ROS were examined by fluorometric DCF-DA kit. The effects of HO and vulpinic acid on actin filaments were determined by tetramethyl rhodamine (TRITC)-phalloidin fluorescence staining. Expression of Tie2 proteins was immunocytochemically analyzed in HO- and vulpinic acid-treated cells. After 24 h, the IC was found to be 215 μM in HUVECs treated with HO. The most effective dose of vulpinic acid against HO-associated damage was found to be 15 μM. Vulpinic acid pretreatment was shown to reduce HO-induced ROS production significantly ( p < 0.05). It was shown that 215 μM of HO 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 HO-treated groups and vulpinic acid pretreatment reduced the expression of this protein. In conclusion, vulpinic acid decreases HO-induced oxidative stress and oxidative stress-related damages in HUVECs. It may be drug candidate in the therapy of atherosclerosis.