Aloe-emodin triggers ROS and Ca 2+ production and decreases the levels of mitochondrial membrane potential of human brain capillary endothelial cells

Abstract

A b s t r a c tThe aim of this hydroxyanthraquinone aloe hCMEC/D3 and to assess the cellular response in the early stage of treatment in order to extend the k capillary endothelial cells hCMEC/D3 were treated with a μM) for a period of 24 hours. The cell viability was determined by MTS assay. The cellul adenosine triphosphate (ATP) levels were evaluated by CellTiter intracellular reactive oxygen species (ROS) were determined by 2',7' H2DCFDA) fluorescence assay. The mitochondrial membrane potential (M using tetramethylrhodamine methyl ester (TMRM) staining, while Fluo the intracellular free Ca using the Arrays Twenty µM, decreased the cell viability as well as the intracellular ATP levels in a dose manner. Increased ROS production and disruption of the have a increased intracellular calcium levels. Our results collectively indicate that AE inhibits proliferation of human brain micro cells via a mechanism involving ROS mitochondrial damage.