The inhibitory effect and mechanism of luteolin 7-glucoside on rat aortic vascular smooth muscle cell proliferation
The inhibitory effect and mechanism of luteolin 7-glucoside on rat aortic vascular smooth muscle cell proliferation
复制标题
DOI：
10.1007/bf02977471
复制
发表时间：
2006-01-01
影响因子：
6.7
通讯作者：
Yun, YP
中科院分区：
文献类型：
--
作者：
Kim, TJ;Kim, JH;Yun, YP
主动脉血管平滑肌细胞(VSMCs)的异常增殖在动脉粥样硬化和血管成形术后再狭窄的发病机制中起核心作用，也可能在高血压的发生发展中起重要作用。本研究旨在探讨木犀草素7-葡萄糖苷(L7G)对血小板衍生生长因子(PDGF)-BB诱导的VSMC增殖的抑制作用及其机制。L7G对PDGF-BB诱导的VSMCs增殖和DNA合成有明显的抑制作用，且呈浓度依赖性。L7G预育可显著抑制PDGF-BB诱导的细胞外信号调节蛋白1/2(ERK1/2)、Akt和磷脂酶C(PLC)-γ1的激活。而L7G对PDGF-BB诱导的PDGF-P受体酪氨酸激酶的磷酸化几乎没有影响。这些结果提示L7G通过阻断PLC-Gamma 1、Akt和ERK1/2的磷酸化来抑制PDGF-BB诱导的VSMCs的增殖。
The abnormal proliferation of aortic vascular smooth muscle cells (VSMCs) plays a central role in the pathogenesis of atherosclerosis and restenosis after angioplasty and possibly also in the development of hypertension. The present study was designed to examine the inhibitory effects and the mechanism of luteolin 7-glucoside (L7G) on the platelet-derived growth factor (PDGF)-BB-induced proliferation of VSMCs. L7G significantly inhibited the PDGF-BB-induced proliferation and the DNA synthesis of the VSMCs in a concentration-dependent manner. Pre-incubation of the VSMCs with L7G significantly inhibited the PDGF-BB-induced extracellular signal-regulated kinase 1/2 (ERK1/2), Akt and the phospholipase C (PLC)-gamma 1 activation. However, L7G had almost no affect on the phosphorylation of PDGF-P receptor tyrosine kinase, which was induced by PDGF-BB. These results suggest that L7G inhibits the PDGF-BB-induced proliferation of VSMCs via the blocking of PLC-gamma 1, Akt, and ERK1/2 phosphorylation.