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GW23-e2148
ACTIVATION OF RETINOID X RECEPTOR PROTECTS AGAINST HYPOXIA-REOXYGENATION INDUCED APOPTOSIS AND LOSS OF MITOCHONDRIAL MEMBRANE POTENTIAL IN H9C2 RAT VENTRICULAR CELLS
  1. Peiren Shan,
  2. Zhouqing Huang,
  3. Weijian Huang
  1. Department of Cardiology, the First Affiliated Hospital of Wenzhou Medical College

    Abstract

    Objectives Retinoid X receptor (RXR) plays a central role in the regulation of intracellular receptor signalling. To determine the effect of activating RXR on rat cardiomyocytes apoptosis and the loss of mitochondrial membrane potential in hypoxia-reoxygenation induced oxidative injury.

    Methods The model of hypoxia/reoxygenation (H/R) injury was established through hypoxia for 6 h and reoxygenation for 4 h in cardiomyocytes of H9c2, We measured the survival rate by Typan blue exclusion, apoptosis rate of cardiomyocytes by FACS analysis, and mitochondrial membrane potential by JC-1 fluorescent probe. All measurement data were expressed as mean±SD of mean, and statistically analysed using one-way ANOVA analysis and Dunnett test. Differences were considered significant when P was<0.05.

    Results We showed that the RXR agonist 9-cis retinoid acid (9-c RA) protected cells from H/R-induced cell injury and loss of mitochondrial membrane potential, and the protective effect of 9-c RA against H/R was abolished when pretreated with HX531 (RXR pan-antagonist).

    Conclusions Activating RXR inhibited apoptosis and prevented the loss of mitochondrial membrane potential induced by H/R injury in rat cardiomyocytes H9c2, which suggests that stabilisation of mitochondrlal membrane potential may be involved in the protection of activating RXR against oxidative stress in H9c2.

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