کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5830626 | 1559081 | 2009 | 7 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Cardiovascular PharmacologyBerberine-induced decline in circulating CD31+/CD42â microparticles is associated with improvement of endothelial function in humans Cardiovascular PharmacologyBerberine-induced decline in circulating CD31+/CD42â microparticles is associated with improvement of endothelial function in humans](/preview/png/5830626.png)
Elevated circulating endothelial microparticles (EMPs) are associated with endothelial dysfunction. This study is to investigate whether berberine-induced fall in circulating EMPs facilitates improvement of endothelial function in healthy subjects. Fourteen healthy subjects received 1-month berberine therapy (1.2 g/d) and 11 healthy subjects served as control. Circulating EMPs were measured by flow cytometric analysis before and after therapy. Brachial artery endothelium-dependent and -independent function was assessed by flow-mediated vasodilation (FMD) and sublinqual nitroglyceride-mediated vasodilation (NMD). In vitro, human umbilical vein endothelial cells (HUVECs) were stimulated by EMPs (106/ml) with or without the presence of berberine (10 μM). Intracellular endothelial nitric oxide synthase (eNOS) protein expression was detected by flow cytometry. After berberine therapy, circulating CD31+/CD42â microparticles were reduced, which was in parallel with the improvement of flow-mediated vasodilation while nitroglyceride-mediated vasodilation kept unchanged. A robust relationship was found between drop of circulating CD31+/CD42â microparticles and increased flow-mediated vasodilation. The EMPs in vitro led to diminished eNOS protein expression in HUVECs and this EMP-mediated detrimental effect was markedly inhibited by berberine. Berberine-induced decline in circulating CD31+/CD42â microparticles contributes to upregulation of endothelial function in healthy subjects. Deceasing EMPs may be a novel therapeutic target for the improvement of endothelial dysfunction in humans.
Journal: European Journal of Pharmacology - Volume 614, Issues 1â3, 1 July 2009, Pages 77-83