Objective To observe the role of ALDH2 on cardiac myocytes variation of reactive oxygen species (ROS), apoptosis and mitogen-activated protein kinases (MAPK) signal route under hypoxia. Methods Cultured cardiomyocytes of neonatal rats were used. Hypoxia was imposed to the cardiomyocytes with or without daidzin pretreatment. ROS was measured by C400, apoptosis by the DeadEndSUP>TM/SUP>TUNEL system and MAPK signal pathway by Western blotting. Each group was dealt with more than three times. Results Compared to hypoxia group, that aldehyde dehydrogenase2(ALDH2) specifically inhibited by pretreated daidzin had a high frequency of ROS, apoptosis and an increased activation of MAPK signal enzymes including phosphorylated ERK1/2, JNK and P38Conclusion The cardiac myocytes variation of ROS, apoptosis and MAPK signal path resulting from hypoxia had a close relation with ALDH2 Myocytes showed decreased tolerance to hypoxia after ALDH2 specifically inhibited by daidzin. ALDH2 prevents hypoxia myocardial in