{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,18]],"date-time":"2026-04-18T05:33:28Z","timestamp":1776490408615,"version":"3.51.2"},"reference-count":33,"publisher":"Canadian Science Publishing","issue":"7","license":[{"start":{"date-parts":[[2010,7,1]],"date-time":"2010-07-01T00:00:00Z","timestamp":1277942400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[2010,7]]},"abstract":"<jats:p> It has been shown that angiotensin\u00a0II (Ang\u00a0II) 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\u00a0weeks with apocynin (Apo) or captopril (Cap). Measures of cardiac hypertrophy were evaluated. Treatment with Cap or Apo reduced the left ventricle\u2009\/\u2009body 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\u00a0II levels and inhibited expression of p22<jats:sup>phox<\/jats:sup> and p67<jats:sup>phox<\/jats:sup> in LVs. In conclusion, local expression of Ang\u00a0II 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. <\/jats:p>","DOI":"10.1139\/y10-063","type":"journal-article","created":{"date-parts":[[2010,7,22]],"date-time":"2010-07-22T19:28:05Z","timestamp":1279826885000},"page":"745-752","source":"Crossref","is-referenced-by-count":22,"title":["Apocynin attenuates pressure overload-induced cardiac hypertrophy in rats by reducing levels of reactive oxygen species"],"prefix":"10.1139","volume":"88","author":[{"given":"Jinjun","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Physiology and Pathophysiology, School of Medicine, Xi\u2019an Jiaotong University, Xi\u2019an 710061, Shaanxi, China."},{"name":"Department of Pharmacology, School of Medicine, Xi\u2019an Jiaotong University, Xi\u2019an 710061, Shaanxi, China."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Juan","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pathophysiology, School of Medicine, Xi\u2019an Jiaotong University, Xi\u2019an 710061, Shaanxi, China."},{"name":"Department of Pharmacology, School of Medicine, Xi\u2019an Jiaotong University, Xi\u2019an 710061, Shaanxi, China."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wenjiao","family":"An","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pathophysiology, School of Medicine, Xi\u2019an Jiaotong University, Xi\u2019an 710061, Shaanxi, China."},{"name":"Department of Pharmacology, School of Medicine, Xi\u2019an Jiaotong University, Xi\u2019an 710061, Shaanxi, China."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yuanxi","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pathophysiology, School of Medicine, Xi\u2019an Jiaotong University, Xi\u2019an 710061, Shaanxi, China."},{"name":"Department of Pharmacology, School of Medicine, Xi\u2019an Jiaotong University, Xi\u2019an 710061, Shaanxi, China."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yubai","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pathophysiology, School of Medicine, Xi\u2019an Jiaotong University, Xi\u2019an 710061, Shaanxi, China."},{"name":"Department of Pharmacology, School of Medicine, Xi\u2019an Jiaotong University, Xi\u2019an 710061, Shaanxi, China."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Weijin","family":"Zang","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pathophysiology, School of Medicine, Xi\u2019an Jiaotong University, Xi\u2019an 710061, Shaanxi, China."},{"name":"Department of Pharmacology, School of Medicine, Xi\u2019an Jiaotong University, Xi\u2019an 710061, Shaanxi, China."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","reference":[{"key":"rg1\/ref1","doi-asserted-by":"publisher","DOI":"10.1097\/FJC.0b013e318177090d"},{"key":"rg2\/ref2","doi-asserted-by":"publisher","DOI":"10.1097\/FJC.0b013e318046f34a"},{"key":"rg3\/ref3","first-page":"S57","volume":"23","author":"Boccanelli A.","year":"2006","journal-title":"G. 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