RGD Reference Report - Magnolol Depresses Urotensin II-Induced Cell Proliferation in Rat Cardiac Fibroblasts. - Rat Genome Database

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Magnolol Depresses Urotensin II-Induced Cell Proliferation in Rat Cardiac Fibroblasts.

Authors: Liou, JY  Chen, YL  Loh, SH  Chen, PY  Hong, CY  Chen, JJ  Cheng, TH  Liu, JC 
Citation: Liou JY, etal., Clin Exp Pharmacol Physiol. 2009 Jan 17.
RGD ID: 2306809
Pubmed: PMID:19207719   (View Abstract at PubMed)
DOI: DOI:10.1111/j.1440-1681.2009.05144.x   (Journal Full-text)

1. Accumulating evidence suggests that oxidative stress plays a key role in the development of cardiac fibrosis. Urotensin II (U-II) has been reported to play an important role in cardiac remodeling and fibrosis. We have recently demonstrated the involvement of reactive oxygen species (ROS) production in U-II-induced cardiac fibroblast proliferation. Magnolol is an antioxidant compound extracted from the cortices of Magnolia officinalis. Thus, it is feasible that magnolol may attenuate cardiac fibroblast proliferation by inhibiting ROS production. Therefore, the aims of this study were to determine whether magnolol alters U-II-induced cell proliferation and to identify the putative underlying signaling pathways in rat cardiac fibroblasts. 2. Cultured rat cardiac fibroblasts were pretreated with magnolol and then stimulated with U-II, following which cell proliferation and endothelin-1 (ET-1) protein secretion was examined. The effect of magnolol on U-II-induced ROS formation and extracellular signal-regulated kinase (ERK) phosphorylation were examined to elucidate the intracellular mechanism by which magnolol influences cell proliferation and ET-1 expression. 3. U-II (30 nM) stimulated cell proliferation, ET-1 protein secretion, and ERK phosphorylation, all of which were inhibited by magnolol (10 muM). Similar to the antioxidant N-acetyl-cysteine (NAC; 5 mM), magnolol (10 muM) also inhibited U-II-increased ROS formation. 4. In sum, our results suggest that magnolol inhibits cardiac fibroblast proliferation by interfering with the generation of ROS. Thus, this study provides important new insights into the molecular pathways involved, which may contribute to our understanding of the effects of magnolol on the cardiovascular system.

Objects referenced in this article
Gene Uts2 urotensin 2 Rattus norvegicus

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