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Mechanism of Aldehyde Dehydrogenase-2 Regulated Human Endothelial Progenitor Cells Oxidative Stress Reaction / 中国循环杂志
Chinese Circulation Journal ; (12): 502-507, 2016.
Artículo en Chino | WPRIM | ID: wpr-489982
ABSTRACT

Objective:

To investigate the role of aldehyde dehydrogenase-2 (ALDH-2) for regulating human endothelial progenitor cells (EPCs) oxidative stress reaction and its mechanism.

Methods:

Human EPCs were isolated from peripheral blood of healthy adults and the cells were cultured in 4 groups①Blank control group,②Alda-1 group, the cells were treated by 1μmol/L Alda-1, a speciifc activator of ALDH-2,③tBHP (10μg/ml) group and④Alda-1 pretreatment+tBHP group. EPCs reactive oxygen species (ROS) levels were evaluated by DCFH-DA staining, mitochondrial membrane potentials were detected by JC-1 method, migration capacity was measured by transwell chamber method and the activation of p38 signal pathway was examined by Western blot analysis.

Results:

Compared with Blank control group, ROS levels in tBHP group and Alda-1 pretreatment+tBHP group were (441.7 ± 24.8) % and (237.4 ± 12.0) %, allP<0.05. In Blank control group, tBHP group and Alda-1 pretreatment+tBHP group, the proportion of EPCs lost their mitochondrial membrane potentials were (5.7 ± 2.1) %, (81.7 ± 3.7) % and (37.4 ± 3.2) % respectively, allP<0.05; the number of EPCs migration were (108 ± 9)/HP, (22 ± 4)/HP and (67 ± 7)/HP respectively, allP<0.05. Compared with Blank control group, the activation of p38 signal pathway increased to (259.1 ± 7.7) % in tBHP group, while it was reduced to (186.4 ± 8.0) % in Alda-1 pretreatment+tBHP group.

Conclusion:

ALDH-2 could reduce ROS level in human EPCs, it may decrease mitochondrial membrane damage, protect migration which might be related to p38 signal pathway.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Circulation Journal Año: 2016 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Circulation Journal Año: 2016 Tipo del documento: Artículo