Gallic acid (GA) found in various plants, fruits and foods has various biological effects including apoptosis. However, little is known about the relationship between reactive oxygen species (ROS) and p38 signaling in GA-treated endothelial cells (ECs). In this study, we investigated the effects of p38 inhibitor on GA-induced calf pulmonary artery endothelial cells (CPAEC) and human umbilical vein endothelial cell (HUVEC) death in view of ROS and glutathione (GSH). GA inhibited the growth of both ECs and induced apoptosis, which was accompanied by the loss of mitochondrial membrane potential (MMP; ΔΨm). The susceptibility of CPAEC to GA is higher than that of HUVEC. GA differently increased or decreased ROS levels in ECs. GA increased GSH depleted cell numbers in ECs. p38 inhibitor seemed to enhance cell growth inhibition and cell death in GA-treated ECs. This inhibitor increased or decreased ROS levels in GA-treated ECs. p38 inhibitor to some extent enhanced GSH depletion in GA-treated CPAEC but it clearly increased GSH depletion cell numbers in GA-treated and -untreated HUVEC. In conclusion, p38 inhibitor appeared to enhance growth inhibition and death in GA-treated ECs, which were partially influenced by the changes of ROS and GSH depletion levels.

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