Inhibited proliferation of human umbilical artery smooth muscle cells by xanthinol nicotinate.

Vascular smooth muscle cell proliferation is a key event in the development of hypertension, instant restenosis and other cardiac disorders. Inhibition of this proliferation could lead to better prevention and treatment of these diseases. This study was designed to investigate the effects and mechanisms of different concentrations of xanthinol nicotinate (XN) on human umbilical artery smooth muscle cell (HUASMC) proliferation in vitro. HUASMCs were cultured by the tissue adherent method, passaged three times, and then identified by immunohistochemistry. HUASMCs were then treated with different concentrations of XN (0, 2.76, 27.6 or 276 µM), and a 3-(4,5-dimethylthiazol-2yl)-2, 5-diphenyltetrazolium bromide (MTT) assay was used to detect the inhibition of HUASMC proliferation. The levels of platelet-derived growth factor receptor (PDGFR) mRNA and protein (PDGFR-β) were detected on the cell membrane of these treated HUASMCs using RT-PCR and Western blot analysis, respectively. After culturing and passaging three times, 90 % of the cultured cells were identified as HUASMCs by immunohistochemistry. HUASMC proliferation was inhibited by XN in a dose-dependent manner (P < 0.05). Furthermore, XN dose-dependently decreased the PDGFR mRNA and PDGFR-β levels on the cell membranes of HUASMCs (P < 0.05). Thus, the results suggest that XN could become a potent therapeutic agent for regulating VSMC-associated vascular disease such as cardiovascular disease and restenosis after angioplasty.