Astaxanthin protecting myocardial cells from hypoxia/reoxygenation injury by regulating miR-138/HIF-1α axis

Y.-S. Gai, Y.-H. Ren, Y. Gao, H.-N. Liu

Department of Cardiology, Yantaishan Hospital, Shandong, P.R. China. dhdsym@sina.cn

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• Cardiology

OBJECTIVE: To investigate astaxanthin (AST) protecting myocardial cells from hypoxia/reoxygenation (H/R) injury by regulating miR-138/HIF-1α axis.

MATERIALS AND METHODS: Myocardial cells were collected and divided into a control group, a H/R group, and a H/R+AST group. The H/R injury model was established, and cells in the H/R+AST group were given AST before modeling. The cell survival rate, contents of myocardial enzymes, and apoptosis were detected.

RESULTS: The survival rate in the H/R group reduced and was lower than that in the H/R+AST group (p<0.05). Compared with the control group, activities of myocardial enzymes significantly increased in the H/R group but those were inhibited in the H/R+AST group (p<0.05). The apoptotic rate in the H/R group significantly increased compared with the control group but that significantly decreased compared with the H/R+AST group (p<0.05). The expression of cleaved caspase-9 and caspase-3 increased in the H/R group (p<0.05), and was higher than that in the H/R+AST group (p<0.05). The expression levels of miR-138 and HIF-1α were detected. MiR-138 level significantly decreased in the H/R group but increased in the H/R+AST group (p<0.05). Compared with the control group, HIF-1α content significantly increased in the H/R group but that was significantly inhibited in the H/R+AST group (p<0.05). The Luciferase reporter gene assay confirmed that HIF-1α was the target gene of miR-138. After miR-138 mimics and HIF-1α siRNA were transfected into myocardial cells, the cell survival rate significantly increased, and activities of myocardial enzymes were significantly inhibited in the H/R+AST+miR-138 mimics and H/R+AST+HIF-1α siRNA groups (p<0.05). The apoptotic rate significantly decreased, and contents of cleaved caspase-9 and caspase-3 were significantly inhibited in the miR-138 mimics and HIF-1α siRNA groups (p<0.05).

CONCLUSIONS: AST can exert a protective function in myocardial cells via regulating the expression of miR-138/HIF-1α axis.

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