p38 inhibitor enhances growth inhibition and death in gallic acid-treated endothelial cells
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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Document Type: Research Article
Affiliations: Department of Pediatric Dentistry, School of Dentistry, Institute for Medical Sciences, Chonbuk National University, JeonJu 561-180, Republic of Korea
Publication date: January 1, 2010
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The International Journal of Molecular Medicine aims to provide an insight for researchers within the community in regard to developing molecular tools and identifying molecular targets for the diagnosis and treatment of a diverse number of human diseases.
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