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  • Title: [Effects of acrolein on apoptosis of H9c2 cardiacmyocytes with hypoxia/reoxygenation injury].
    Author: Shao QR, Du D, He Y, Wu XH, Huang W, Xing ZH.
    Journal: Sichuan Da Xue Xue Bao Yi Xue Ban; 2012 Jul; 43(4):483-7. PubMed ID: 22997880.
    Abstract:
    OBJECTIVE: To determine the cytotoxic effects of acrolein on hypoxia/reoxygenation (H/R) injury in H9c2 cardiacmyocytes and investigate the intracellular signaling pathways. METHODS: Hypoxia/reoxygenation (H/R) injury model was established with H9c2 cells. The H9c2 cells were divided into four groups, the control group, acrolein group (ACR), H/R group, acrolein + H/R group (ACR + H/R). H9c2 cells pretreated with or without acrolein (10 micromol/L) for 30 min were exposed to 2 h hypoxia and 16 h reoxygenation. The effect of acrolein on the cellular viability and apoptosis of H9c2 cells was measured by MTT assay, DAPI stainning and flow cytometry (FCM) respectively. The expression of apotosis-related proteins (cytochrome c, caspase 9 and caspase 3) in the H9c2 cells was detected by Western blot. RESULTS: Compared with mere H/R treatment, the decrease in cell viability and increase in the number of apoptotic cells in H9c2 cells subjected to H/R were significantly exacerbated in the presence of acrolein (P < 0.05). The liberation of cytochrome c from mitochondria to cytosol, the cleavages of the initiator caspase 9 and the effector caspase 3 have been observed after pretreatment with acrolein followed by H/ R in H9c2 cells. CONCLUSION: Acrolein could aggravate H/R injury and that this effect may be related, in part, to the modification of proteins involved the release of cytochrome c from mitochondria to cytosol and activation of caspases cascade reaction.
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