Apocynin attenuates pressure overload-induced cardiac hypertrophy in rats by reducing levels of reactive oxygen species

Canadian Journal of Physiology and Pharmacology
Jinjun LiuWeijin Zang

Abstract

It has been shown that angiotensin II (Ang II) is involved in cardiac remodeling mediated by NADPH oxidase-dependent reactive oxygen species (ROS). Accordingly, NADPH oxidase-dependent ROS may play a role in cardiac hypertrophy induced by pressure overload. In the present study, we sought to determine whether inhibition of NADPH oxidase prevents cardiac hypertrophy. After abdominal aorta banding to induce cardiac hypertrophy, rats were treated for 8 weeks with apocynin (Apo) or captopril (Cap). Measures of cardiac hypertrophy were evaluated. Treatment with Cap or Apo reduced the left ventricle/body weight ratio (LV/BW), LV transnuclear myocyte diameter, and atrial natriuretic factor (ANF) mRNA expression relative to those of untreated rats subjected to aorta banding. The activity of NADPH oxidase and the ROS levels were decreased in treated animals. Cap, but not Apo, decreased Ang II levels and inhibited expression of p22phox and p67phox in LVs. In conclusion, local expression of Ang II appears to contribute to pressure overload-induced cardiac hypertrophy by upregulating NADPH oxidase expression and promoting ROS synthesis. Inhibition of NADPH oxidase and elimination of ROS may prevent or repair damage due to cardiac hypertrophy.

References

Feb 7, 1998·Proceedings of the National Academy of Sciences of the United States of America·P J PaganoM T Quinn
May 10, 2001·Journal of Molecular and Cellular Cardiology·Y SunK T Weber
May 23, 2003·Journal of the American Society of Nephrology : JASN·Elise CourtoisAntonio López-Farré
Jul 8, 2003·Current Hypertension Reports·Rubin ZhangEfrain Reisin
Feb 26, 2004·Circulation·Melanie MaytinWilson S Colucci
Jul 9, 2004·Journal of Leukocyte Biology·Mark T Quinn, Katherine A Gauss
Aug 27, 2005·Toxicology and Applied Pharmacology·Chiara RigantiDario Ghigo
Sep 21, 2005·Journal of Molecular and Cellular Cardiology·Tamás CsontRichard Schulz
Dec 3, 2005·Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences·Alison CaveAjay M Shah
May 25, 2006·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Sofian JoharAjay M Shah
Jun 13, 2006·Cardiovascular Research·Tamara M Paravicini, Rhian M Touyz
Feb 28, 2007·Clinical and Experimental Pharmacology & Physiology·Micheline M de Resende, José G Mill
Dec 19, 2007·Hypertension·Sabine HeumüllerRalf P Brandes
Feb 16, 2008·Current Opinion in Nephrology and Hypertension·Rajesh KumarKenneth M Baker
Mar 4, 2008·American Journal of Veterinary Research·Masami UechiShigeki Yamano
Jul 4, 2008·Cardiovascular Research·Torsten SchlüterOlaf Grisk
Oct 17, 2008·American Journal of Physiology. Regulatory, Integrative and Comparative Physiology·Niu TianR Davis Manning

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Citations

Jan 28, 2014·Pharmacology & Therapeutics·Karina HuynhRebecca H Ritchie
Jul 3, 2015·Antioxidants & Redox Signaling·Kazufumi HiranoA Richard Rutter
Mar 13, 2012·Vascular Pharmacology·Agata SchrammTomasz J Guzik
Mar 27, 2015·Antioxidants & Redox Signaling·Miranda M SungJason R B Dyck
Oct 10, 2012·International Journal of Cardiology·Lu-Yu ZhouPei-Feng Li
Jul 23, 2013·Biochimica Et Biophysica Acta·Astrid SchrammelBernd Mayer
Mar 29, 2014·Nutrition, Metabolism, and Cardiovascular Diseases : NMCD·I OnakpoyaM Thompson
Dec 20, 2017·Molecular and Cellular Biochemistry·Nikhat SaleemShyamal K Goswami
Jun 9, 2020·Oxidative Medicine and Cellular Longevity·Rossella D'OriaFrancesco Giorgino
Jan 9, 2019·Frontiers in Physiology·Klaus-Dieter SchlüterRainer Schulz

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