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The aim of the present study was to determine whether breviscapine attenuates cardiac hypertrophy induced by angiotensin II (Ang II) in cultured neonatal rat cardiac myocytes in vitro and pressure\u2010overload\u2010induced cardiac hypertrophy in mice in vivo. Our data demonstrated that breviscapine (2.5\u201315\u2009\u00b5M) dose\u2010dependently blocked cardiac hypertrophy induced by Ang II (1\u2009\u00b5M) in vitro. The results further revealed that breviscapine (50\u2009mg\/kg\/day) prevented cardiac hypertrophy induced by aortic banding as assessed by heart weight\/body weight and lung weight\/body weight ratios, echocardiographic parameters, and gene expression of hypertrophic markers. The inhibitory effect of breviscapine on cardiac hypertrophy is mediated by disrupting PKC\u2010\u03b1\u2010dependent ERK1\/2 and PI3K\/AKT signaling. Further studies showed that breviscapine inhibited inflammation by blocking NF\u2010\u03baB signaling, and attenuated fibrosis and collagen synthesis through abrogating Smad2\/3 signaling. Therefore, these findings indicate that breviscapine, which is a potentially safe and inexpensive therapy for clinical use, has protective potential in targeting cardiac hypertrophy and fibrosis through suppression of PKC\u2010\u03b1\u2010dependent signaling. J. Cell. Biochem. 109: 1158\u20131171, 2010. \u00a9 2010 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcb.22495","type":"journal-article","created":{"date-parts":[[2010,2,1]],"date-time":"2010-02-01T14:04:30Z","timestamp":1265033070000},"page":"1158-1171","source":"Crossref","is-referenced-by-count":41,"title":["Breviscapine protects against cardiac hypertrophy through blocking PKC\u2010\u03b1\u2010dependent 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