School of Pharmacy, Xi'an Jiaotong University, Xi'an 710061, PR China.
School of Pharmacy, Xi'an Jiaotong University, Xi'an 710061, PR China.
Int Immunopharmacol. 2018 Jan;54:103-111. doi: 10.1016/j.intimp.2017.10.017. Epub 2017 Nov 6.
The proliferation, migration and inflammation of vascular smooth muscle cells (VSMCs) contributes to the pathogenesis and progression of atherosclerosis. Paeoniflorin (PF) as active compound in the Rhizoma Atractylodes macrocephala has been used for various diseases like cancer, splenic asthenia, anaphylaxis and anorexia. This study aimed to explore whether and how PF regulated the inflammation, proliferation and migration of VSMCs under ox-LDL stimulation. Here, we found that PF dose-dependently inhibited ox-LDL-induced VSMCs proliferation and migration, and decreased inflammatory cytokines and chemokine overexpression. Mechanistically, PF prevented p38, ERK1/2 and NF-κB phosphorylation, and arrested cell cycle in S phase. Meanwhile, PF regulated the HO-1 and PCNA expression. Furthermore, PF blocked the foam cell formation in macrophages induced by ox-LDL. These results indicate that PF antagonizes the ox-LDL-induced VSMCs proliferation, migration and inflammation through activation of HO-1, cell cycle arrest and then suppression of p38, ERK1/2/MAPK and NF-κB signaling pathways.
血管平滑肌细胞（VSMCs）的增殖、迁移和炎症反应导致动脉粥样硬化的发病和进展。芍药苷（PF）作为白术根茎中的活性化合物，已被用于治疗癌症、脾虚、过敏和厌食等各种疾病。本研究旨在探讨芍药苷是否以及如何调节 ox-LDL 刺激下 VSMCs 的炎症、增殖和迁移。结果发现，芍药苷呈剂量依赖性地抑制 ox-LDL 诱导的 VSMCs 增殖和迁移，并降低炎症细胞因子和趋化因子的过度表达。机制上，芍药苷可阻止 p38、ERK1/2 和 NF-κB 的磷酸化，并使细胞周期停滞在 S 期。同时，芍药苷可调节 HO-1 和 PCNA 的表达。此外，芍药苷可阻止 ox-LDL 诱导的巨噬细胞泡沫细胞的形成。这些结果表明，芍药苷通过激活 HO-1、细胞周期阻滞以及抑制 p38、ERK1/2/MAPK 和 NF-κB 信号通路，拮抗 ox-LDL 诱导的 VSMCs 增殖、迁移和炎症反应。
