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      Sodium tanshinone IIA sulfonate attenuates angiotensin II-induced collagen type I expression in cardiac fibroblasts in vitro.

      Experimental & Molecular Medicine

      pharmacology, Acetylcysteine, Angiotensin II, antagonists & inhibitors, Animals, Blotting, Western, Cells, Cultured, Collagen Type I, metabolism, Drugs, Chinese Herbal, Fibroblasts, drug effects, Free Radical Scavengers, In Vitro Techniques, Matrix Metalloproteinase 1, Myocardium, cytology, NADPH Oxidase, Oxidative Stress, Phenanthrenes, Rats, Rats, Wistar, Reactive Oxygen Species

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          Abstract

          Cardiac fibrosis occurs after pathological stimuli to the cardiovascular system. One of the most important factors that contribute to cardiac fibrosis is angiotensin II (AngII). Accumulating studies have suggested that reactive oxygen species (ROS) plays an important role in cardiac fibrosis and sodium tanshinone IIA sulfonate (STS) possesses antioxidant action. We therefore examined whether STS depresses Ang II-induced collagen type I expression in cardiac fibroblasts. In this study, Ang II significantly enhanced collagen type I expression and collagen synthesis. Meanwhile, Ang II depressed matrix metalloproteinase-1 (MMP-1) expression and activity. These responses were attenuated by STS. Furthermore, STS depressed the intracellular generation of ROS, NADPH oxidase activity and subunit p47(phox) expression. In addition, N-acetylcysteine the ROS scavenger, depressed effects of Ang II in a manner similar to STS. In conclusion, the current studies demonstrate that anti-fibrotic effects of STS are mediated by interfering with the modulation of ROS.

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          Author and article information

          Journal
          19322029
          2721148
          10.3858/emm.2009.41.7.056

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