Magnolol attenuates neointima formation by inducing cell cycle arrest via inhibition of ERK1/2 and NF-κB activation in vascular smooth muscle cells

• Published in: Biochimica et biophysica acta. General subjects Vol. 1830; no. 3; pp. 2619 - 2628
• Main Authors: Karki, Rajendra, Ho, Oak-Min, Kim, Dong-Wook
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 01.03.2013
• Subjects: atherosclerosis; carotid arteries; cell cycle checkpoints; Cell cycle regulator; colorimetry; cyclin-dependent kinase; cyclins; flow cytometry; gene expression; in vitro studies; Magnolol; messenger RNA; mitogen-activated protein kinase; myocytes; Neointima; oral administration; phenotype; phosphorylation; protein synthesis; rats; Restenosis; reverse transcriptase polymerase chain reaction; smooth muscle; transcription factor NF-kappa B; tumor necrosis factor-alpha; Vascular smooth muscle cell; Western blotting; Restenosis; Cell cycle regulator; Magnolol; Vascular smooth muscle cell; Neointima

Endovascular injury induces switching of contractile phenotype of vascular smooth muscle cells (VSMCs) to synthetic phenotype, thereby causing proliferation of VSMCs leading to intimal thickening. The purpose of this study was to assess the effect of magnolol on the proliferation of VSMCs in vitro a...