School of Basic Courses, Guangdong Pharmaceutical University, Guangdong Provincial Key Laboratory of Pharmaceutical Bioactive Substances, Guangzhou Higher Education Mega Center, Guangzhou, China.
School of Traditional Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou, China.
J Cardiovasc Pharmacol. 2018 May;71(5):268-274. doi: 10.1097/FJC.0000000000000567.
Cellular interactions between endothelial cell (EC) and vascular smooth muscle cell (VSMC)/macrophages seem to be greatly changed under inflammatory conditions. Although simvastatin could regulate inflammatory transcription factors in EC and VSMC and also could inhibit leukocyte-endothelium interaction, whether it could modulate VSMC/macrophage functions that are induced by tumor necrosis factor-α (TNF-α)-activated EC remained unclear. The purpose of this study was to investigate the effects of simvastatin on VSMC/macrophage functions, which are induced by TNF-α-activated EC in coculture system in vitro. The results showed that under noncontacting conditions, simvastatin could reduce the proliferation, apoptosis, and TNF-α, IL-6, and vascular endothelial growth factor secretion both in VSMC and macrophage, which is induced by TNF-α-activated EC. And a hypothesis that simvastatin regulates the interactions and the soluble factors between EC and VSMC/macrophages could be drawn. And that might be a potential anti-atherosclerosis mechanism of simvastatin.
细胞间相互作用内皮细胞(EC)和血管平滑肌细胞(VSMC)/巨噬细胞在炎症条件下似乎发生了很大的变化。虽然辛伐他汀可以调节 EC 和 VSMC 中的炎症转录因子,也可以抑制白细胞-内皮细胞相互作用,但它是否可以调节由肿瘤坏死因子-α(TNF-α)激活的 EC 诱导的 VSMC/巨噬细胞功能尚不清楚。本研究旨在探讨辛伐他汀对体外共培养体系中 TNF-α激活的 EC 诱导的 VSMC/巨噬细胞功能的影响。结果表明,在非接触条件下,辛伐他汀可降低由 TNF-α激活的 EC 诱导的 VSMC 和巨噬细胞增殖、凋亡以及 TNF-α、IL-6 和血管内皮生长因子的分泌。可以提出辛伐他汀调节 EC 与 VSMC/巨噬细胞之间相互作用和可溶性因子的假说,这可能是辛伐他汀抗动脉粥样硬化的潜在机制。