Involvement of Oxidative Stress and Down-Regulation of Bcl-2 in Arachidonic Acid-Induced Apoptosis in HUVECs

0IntroductionAraacicdhi,diosn fiocu ancidd p(reAdAo)m i,naanntelsys eantt itahle p sonl-y2u npsoastiutiroante doff actetl-ylular phospholipids . Normal free AAconcentrationin humanblood ranges from5 .8μmol/Lto 49 .3μmol/L1].It is re-leased mostlythroughactivation of phospholipase A2by physi-ological and pathological sti muli2]. Free AAcan be metabo-lizedinto various eicosanoids via specific enzymes such as cy-clooxygenases ( COX) , lipoxygenase and cytochromesP-4503]. During AA met…

Involvement of oxidative stress and down-regulation of Bcl-2 in arachidonic acid-induced apoptosis in HUVECs

Human umbilical vein endothelial cells (HUVECs) were treated with arachidonic acid (AA). After 24 h exposure to AA, typical morphological changes of apoptosis were observed by Giemsa stain and transmission electron microscopy. The apoptotic ratio in HUVECs treated with 50 μmol/L, 100 μmol/L and 150 μmol/I. AA were (20.7±3.6)%, (38.6±4.3)% and (52.5±7.5)% respectively. Contrarily, low concentration of AA (≤25 μmol/L) exerted no influence on cell viability by MTT assay. Intracellular malondialdehyde increased significantly in a dose-dependent manner upon AA treatment and the opposite tendency was found for the reduced glutathione. Western Blots show that apoptosis triggered by AA was associated with the down-regulation of Bcl-2 expression, but not with Bax and p53. Pretreatment with 50 μmol/L α-tocopherol reduced AA-induced oxidative stress and apoptosis, also inhibited the down-regulation of Bcl-2/Bax ratio. These results suggested that high concentration of free AA could induce apoptosis in HUVECs probably via oxidative stress and down-regulation of Bcl-2. Foundation item: Supported by the Natural Science Foundation of Hubei Province (2003ABA188) Biography: WANG Bing-hua (1965-), male, Ph.D. candidate, research direction: vascular biology.