Key result
Cryptotanshinone attenuated cardiac fibrosis in vitro and in vivo by inhibiting Ang II-induced ERK1/2 phosphorylation and the expression of COX-2, NOX-2, and NOX-4.
Cryptotanshinone demonstrates antifibrotic effects in preclinical models of myocardial infarction by downregulating COX-2, NOX-2, and NOX-4 pathways.
Hypothesis-generating for cryptotanshinone in cardiac fibrosis; human trials needed before any clinical consideration.
Cryptotanshinone (CTS), a bioactive constituent extracted from a Chinese traditional herb Danshen (Salvia miltiorrhiza), demonstrates multiple protective effects against cardiovascular diseases. The present study was designed to explore the effects of CTS in vitro by cultured adult rat cardiac fibroblasts stimulated with angiotensin II (Ang II) and in vivo by rats with acute myocardial infarction. Our data showed that in cardiac fibroblasts, CTS attenuated Ang II-induced upregulation of fibronectin, connective tissue growth factor, cyclooxygenase-2, and normalized Ang II-induced upregulation of extracellular signal-regulated kinases 1/2 (ERK1/2). Meanwhile, CTS depressed the Ang II-stimulated upregulation of NAD(P)H oxidase 2 and 4 (NOX-2 and NOX-4) and reactive oxygen species production. Similar results were observed in acute myocardial infarction rats with oral administration of CTS, which relieved the pathological changes accompanying myocardial infarction. In conclusion, CTS may exert antifibrotic effects in vitro by inhibiting Ang II-induced extracellular signal-regulated kinases 1/2 phosphorylation and the expression of cyclooxygenase-2, NOX-2, and NOX-4, and also improved the pathological changes and relieved cardiac fibrosis in vivo.
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Ma et al. (2014) studied Cardiac fibrosis and acute myocardial infarction. Cryptotanshinone (CTS) was evaluated on Attenuation of Ang II-induced upregulation of fibrotic markers, COX-2, NOX-2, NOX-4, and ROS production. Cryptotanshinone attenuated cardiac fibrosis in vitro and in vivo by inhibiting Ang II-induced ERK1/2 phosphorylation and the expression of COX-2, NOX-2, and NOX-4.
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