Bo-Gan-Whan regulates proliferation and migration of vascular smooth muscle cells.
Autor: | Kang Pa Lee, Jai-Eun Kim, Hyuck Kim, Hae Ryong Chang, Dae Won Lee, Won-Hwan Park |
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Předmět: |
ANIMALS
CHEMILUMINESCENCE assay HERBAL medicine HIGH performance liquid chromatography ASIAN medicine PLATELET-derived growth factor RATS RESEARCH funding STATISTICS T-test (Statistics) VASCULAR smooth muscle PLANT extracts DATA analysis DATA analysis software DESCRIPTIVE statistics IN vitro studies ONE-way analysis of variance |
Zdroj: | BMC Complementary & Alternative Medicine; 8/22/2016, Vol. 16, p1-8, 8p, 6 Graphs |
Abstrakt: | Background: Bo-Gan-Whan (BGH), a Korean polyherbal medicine, is used as a hepatoprotective drug. It has six natural sources, and has been demonstrated to have anti-oxidative, anti-cancer, and anti-inflammatory properties; however, its effect on vascular diseases remains unclear. Methods: Cell viability and proliferation assays were employed using an EZ-Cytox Cell Viability Assay Kit. Platelet-derived growth factor (PDGF)-BB-induced vascular smooth muscle cell (VSMC) migration was measured by scratch wound healing assay and Boyden chamber assay. The expression levels of the phosphorylated signaling proteins relevant to proliferation, including extracellular signal-regulated kinase (ERK) 1/2 and p38 mitogen-activated protein kinase (MAPK) were determined by western blot analysis. Chromatogram and mass analysis were employed by Ultra Performance Liquid Chromatography (UPLC) system. Cell prolife ration and migration were also explored using the PDGF-BB-induced aortic sprout assay. Results: BGH (100-500 µg/mL) significantly inhibited the proliferation and migration of PDGF-BB-stimulated VSMCs through the reduced phosphorylation of ERK1/2 and p38 MAPK in comparison to untreated PDGF-BB-stimulated VSMC. Moreover, we identified the paeoniflorin as the major composition of BGH. Conclusions: We suggest that BGH may have an anti-atherosclerosis effect by inhibiting the proliferation and migration of PDGF-BB-stimulated VSMCs through down-regulation of ERK1/2 and p38 MAPK phosphorylation. [ABSTRACT FROM AUTHOR] |
Databáze: | Complementary Index |
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