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      https://www.ias.ac.in/article/fulltext/jbsc/043/05/0857-0865

    • Keywords

       

      Hypoxia-reoxygenation; p38; UCP2; ursolic acid

    • Abstract

       

      Oxidative stress and apoptosis is involved in hypoxia-reoxygenation (H/R) induced myocardial injury. Increased expressionof uncoupling protein 2 (UCP2), a cationic carrier protein, has protective effect against H/R injury. The present study aimedto find candidate drugs for H/R induced cardiac damage by identifying compounds regulating UCP2 expression. Here,among six natural compounds, ursolic acid (UA) had the most significant induction effect on UCP2 expression in H9c2cells under H/R conditions. Subsequently, we found that UA significantly attenuated cell apoptosis and Caspase 3 activity,but increased nitric oxide (NO) release under H/R conditions. Additionally, UA pretreatment also decreased reactiveoxygen species (ROS) production and malondialdehyde (MDA) content, but increased superoxide dismutase (SOD)activity. H/R caused a notable increase in the phosphorylation of p38, which was weakened by UA pretreatment. Moreover,p38 inhibitor (SB203580) showed the similar effects on H/R cells as UA pretreatment, while UCP2 knockdown had thereverse biological effects. More importantly, the effects of UA or p38 inhibitor exposure were partially rescued by UCP2knockdown. Collectively, our data suggested the functions of UA on UCP2 expression and on the protection of H/RstimulatedH9c2 cells may be attributed to p38 signaling pathway.

    • Author Affiliations

       

      MIN CHEN1 XIAODONG WANG1 BO HU1 JIAN ZHOU1 XIN WANG1 WEI WEI1 HUA ZHOU1

      1. Department of Cardiovascular Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China
    • Dates

       
  • Journal of Biosciences | News

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