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Decreased expression of mitochondrial aldehyde dehydrogenase‐2 induces liver injury via activation of the mitogen‐activated protein kinase pathway

The aim of this study was to determine the role of ALDH2 in the injury of liver from brain‐dead donors. Using brain‐dead rabbit model and hypoxia model, levels of ALDH2 and apoptosis in tissues and cell lines were determined by Western blot, flow cytometry (FCM), and transferase (TdT)‐mediated biotin‐16‐dUTP nick‐end labeling (TUNEL) assays. After the expression of ALDH2 during hypoxia had been inhibited or activated, the accumulations of 4‐hydroxynonenal (4‐HNE) and molecules involved in mitogen‐activated protein kinase (MAPK) signaling pathway were analyzed using ELISA kit and Western blot. The low expression of phosphorylated ALDH2 in liver was time‐dependent in the brain‐dead rabbit model. Immunohistochemistry showed ALDH2 was primarily located in endothelial, and the rates of cell apoptosis in the donation after brain‐death (DBD) rabbit groups significantly increased with time. Following the treatment of inhibitor of ALDH2, daidzein, in combination with hypoxia for 8 h, the apoptosis rate and the levels of 4‐HNE, P‐JNK, and cleaved caspase‐3 significantly increased in contrast to that in hypoxic HUVECs; however, they all decreased after treatment with Alda‐1 and hypoxia compared with that in hypoxic HUVECs (P < 0.05). Instead, the levels of P‐P38, P‐ERK, P‐JNK, and cleaved caspase‐3 decreased and the ratio of bcl‐2/bax increased with ad‐ALDH2 (106pfu/ml) in combination with hypoxia for 8 h, which significantly alleviated in contrast to that in hypoxic HUVECs. We found low expression of ALDH2 and high rates of apoptosis in the livers of brain‐dead donor rabbits. Furthermore, decreased ALDH2 led to apoptosis in HUVECs through MAPK pathway.