Effects of total flavones from Dendranthema morifolium on vasocontraction and proliferation of vascular smooth muscle cells

Jin,Hong‑Feng; Liu,Xiao‑Wei; Tang,Yi‑Ming; Tang,Li‑Jiang; Wang,Ya‑Li; Du,Chang‑Qing

doi:10.3892/mmr.2015.4576

Effects of total flavones from Dendranthema morifolium on vasocontraction and proliferation of vascular smooth muscle cells

Authors:
- Hong‑Feng Jin
- Xiao‑Wei Liu
- Yi‑Ming Tang
- Li‑Jiang Tang
- Ya‑Li Wang
- Chang‑Qing Du
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Affiliations: Department of Cardiology, Zhejiang Hospital, Hangzhou, Zhejiang 310013, P.R. China, Department of Cardiology, The First Clinical Medical Institute of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China
Published online on: November 19, 2015 https://doi.org/10.3892/mmr.2015.4576
Pages: 989-993

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Abstract

Pharmacological studies have shown that the active components in Dendranthema morifolium exhibit protective effects against ischemia/reperfusion injury; however, its pharmacological action on blood vessels has not yet been investigated. The purpose of the present study was to assess the effects of the total flavones extracted from D. morifolium (Ramat.) Tzvel. cv. Hangju (FDM) on the vasocontraction and proliferation of vascular smooth muscle cells (VSMCs). The tension of rat thoracic aortic rings was measured using a mechanical force transducer attached to a recording system. FDM induced a dose‑dependent relaxation of rings with endothelium pre‑contracted by either phenylephrine (PE; 10‑6 mol/l) or a high concentration of potassium chloride (KCl; 60 mmol/l). FDM did not significantly affect the vasorelaxant effects on mechanically removed endothelium. In endothelium‑denuded aortic rings depolarized by 60 mmol/l KCl, FDM inhibited the contraction induced by Ca2+. FDM reduced the transient contraction caused by PE in a Ca2+‑free solution, but did not affect the contraction induced by phorbol ester. Furthermore, FDM inhibited the proliferation of VSMCs with or without growth stimulation by insulin. In conclusion, that the vasorelaxation induced by FDM in rat aortic rings is not dependent on the endothelium but is mediated via a reduction of the influx of extracellular Ca2+ through the voltage‑dependent and receptor‑operated channels and via the inhibition of the release of intracellular Ca2+ in VSMCs. The anti‑proliferative activity of FDM suggests that it may be beneficial in inhibiting atherosclerosis.

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