Artemisinin attenuates platelet-derived growth factor BB-induced migration of vascular smooth muscle cells

• Published in: Nutrition research and practice Vol. 8; no. 5; pp. 521 - 525
• Main Authors: Lee, Kang Pa, Park, Eun-Seok, Kim, Dae-Eun, Park, In-Sik, Kim, Jin Tack, Hong, Heeok
• Format: Journal Article
• Language: English
• Published: Korea (South) 한국영양학회 01.10.2014; The Korean Nutrition Society and the Korean Society of Community Nutrition
• Subjects: Original Research; 생활과학; ERK1/2; vascular smooth muscle cells; MMP9; platelet-derived growth factor-BB; Artemisinin
• ISSN: 1976-1457; 2005-6168
• DOI: 10.4162/nrp.2014.8.5.521

Artemisinin (AT), an active compound in Arternisia annua, is well known as an anti-malaria drug. It is also known to have several effects including anti-oxidant, anti-inflammation, and anti-cancer activities. To date, the effect of AT on vascular disorders has not been studied. In this study, we investigated the effects of AT on the migration and proliferation of vascular smooth muscle cells (VSMC) stimulated by platelet-derived growth factor BB (PDGF-BB). Aortic smooth muscle cells were isolated from Sprague-Dawley rats. PDGF-BB stimulated VSMC migration was measured by the scratch wound healing assay and the Boyden chamber assay. Cell viability was determined by using an EZ-Cytox Cell Viability Assay Kit. The production of reactive oxygen species (ROS) in PDGF-BB stimulated VSMC was measured through H2DCF-DA staining. We also determined the expression levels of signal proteins relevant to ROS, including measures of extracellular signal-regulated kinase (ERK) 1/2 measured by western blot analysis and matrix metalloproteinase (MMP) 9 measured by reverse transcription-polymerase chain reaction (RT-PCR). AT (10 µM and 30 µM) significantly reduced the proliferation and migration of PDGF-BB stimulated VSMC in a dose-dependent manner. The production of ROS, normally induced by PDGF-BB, is reduced by treatment with AT at both concentrations. PDGF-BB stimulated VSMC treated with AT (10 µM and 30 µM) have reduced phosphorylation of ERK1/2 and inhibited MMP9 expression compared to untreated PDGF-BB stimulated VSMC. We suggest, based on these results, that AT may exert an anti-atherosclerotic effect on PDGF-BB stimulated VSMCs by inhibiting their proliferation and migration through down-regulation of ERK1/2 and MMP9 phosphorylation.