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[Protective effect of ecdysterone against sodium arsenite-induced endothelial cell apoptosis]
1Department of Cardiothoracic Surgery, Nanfang Hospital, First Military Medical University, Guangzhou 510515, China. wuxu5888@fimmu.edu.cn
Objective:
To study whether ecdysterone (EDS) inhibits apoptosis of endothelial cells.
Methods:
In the model of sodium arsenite (Ars)-induced endothelial cell apoptosis, the effect of EDS at varied dosages (50, 200, 800 mg/L) on cell apoptosis was observed by measuring the number of apoptotic endothelial cells, intracellular adhesion molecule-1 (ICAM-1) and the oxidative state (OS).
Results:
Ars at the dosages of 40, 80, 160 mmol/L was capable of causing an increase in the number of apoptotic endothelial cells in vitro, and 160 mmol/L Ars exhibited the strongest effect. EDS was shown to exert influence on the apoptosis-inducing effect of Ars, which decreased the apoptotic cell number at the dosage of 50 and 200 mg/L, but a contrary effect occurred while at the dosage of 800 mg/L. Meanwhile EDS (50, 200 mg/L) inhibited the increase of ICAM-1 expression in the endothelial cells in response to Ars, but failed to significantly elevate the low OS induced by Ars (P>0.05).
Conclusion:
Ars induces endothelial cell apoptosis dose-dependently, and in a similar manner, EDS produces influence on the apoptosis-inducing action of Ars. EDS (50, 200 mg/L) may decrease the apoptotic endothelial cell number and lower the Ars-induced increase of ICAM-1 expression, demonstrating its protective effect on the endothelial cells against apoptosis.
