Selective inhibition of p38alpha MAPK improves cardiac function and reduces myocardial apoptosis in rat model of myocardial injury.

@article{Li2006SelectiveIO,
  title={Selective inhibition of p38alpha MAPK improves cardiac function and reduces myocardial apoptosis in rat model of myocardial injury.},
  author={Zhihe Li and Jing Ying Ma and Irene Kerr and Sarvajit Chakravarty and Sundeep Dugar and George F. Schreiner and Andrew Asher Protter},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2006},
  volume={291 4},
  pages={
          H1972-7
        }
}
  • Zhihe Li, J. Ma, +4 authors A. Protter
  • Published 2 June 2006
  • Biology, Medicine
  • American journal of physiology. Heart and circulatory physiology
p38 MAPK is activated during heart diseases that might associate with myocardial damage and deterioration of cardiac function. In a rat model of myocardial injury, we have investigated cardioprotective effects of the inhibition of p38 MAPK using a novel, orally available p38alpha MAPK inhibitor. Rats were treated with N(omega)-nitro-l-arginine methyl ester (l-NAME, 40 mg.kg(-1).day(-1)) in drinking water plus 1% salt for 14 days and ANG II (0.5 mg.kg(-1).day(-1)) for 3 days. A selective… 
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It is demonstrated that IL-33 suppresses inflammatory responses and improved LV function and remodeling by inhibiting the p38 MAPK and NF-κB pathways.
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It is concluded that insulin protects myocardium against ischemiareperfusion injury when given prior to ischemia or reperfusion, and activation of p38 MAPK abolishes insulin’s cardioprotective effect.
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TLDR
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TLDR
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TLDR
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