[Activation of aldehyde dehydrogenase 2 alleviates H O -induced injury in cardiomyocytes].

Objective: To investigate the changes of aldehyde dehydrogenase 2 (ALDH2) expression in H O inducedcardiomyocytes oxidative stress injury.

Methods: Cultured H9C2 cardiomyocytes were exposed to H O -inducedoxidative stress and the effects of the ALDH2 agonist Alda-1 and ALDH2 inhibitor Daidzin were tested on the stress level ofthe exposed cells. MTT colorimetric assay was used to assess the cell viability after the treatments. The oxidative stress level inthe myocardial cells was detected using DHE fluorescence staining, and the activity and protein level of ALDH2 were detectedwith spectrophotometry and Western blotting.

Results: Compared with normal control cells, Alda-1 treatment did notsignificantly affect the cell viability, oxidative stress level, or ALDH2 activity and protein level. H O exposure significantlylowered the cell activity and ALDH2 activity and protein expression and increased the oxidative stress level; Alda-1 treatmentobvious antagonized the effects of H O . Blocking ALDH2 with Daidzin produced similar effects to H O exposure on theviability, oxidative stress level, and ALDH2 activity and expression in the myocardial cells.

Conclusions: H O exposure lowersthe activity and reduces the protein expression of ALDH2 in cardiomyocyte H9C2 cells, and activation of ALDH2 can alleviateH O -induced oxidative stress in the cells.