Translational Medicine Research Center, Shanxi Medical University, Taiyuan, Shanxi, 030001, People's Republic of China.
Key Laboratory of Cellular Physiology, Ministry of Education, Shanxi Medical University, Taiyuan, Shanxi, 030001, People's Republic of China.
Inflammation. 2017 Aug;40(4):1450-1459. doi: 10.1007/s10753-017-0588-3.
Genistein plays an important role in the prevention of atherosclerosis. However, the underlying mechanisms have not been fully investigated. In this study, human umbilical vein endothelial cells (HUVECs) were pretreated with genistein (10, 100, and 1000 nM) for 6 h and then exposed to ox-LDL (50 mg/L) for another 24 h. Results showed that ox-LDL induced the expressions of E-selectin, P-selectin, monocyte chemotactic protein-1, interleukin-8, vascular adhesion molecule-1, and intercellular adhesion molecule-1, which were counteracted by genistein. The inhibitory effect was further enhanced with the augment of genistein (10, 100, and 1000 nM). Further analyses demonstrated the effect of genistein was associated with reducing miR-155 and elevating SOCS1, and miR-155 mimics or SOCS1 siRNA acted similarly in genistein ameliorating inflammation. Moreover, the effect of genistein was accompanied with the inhibition of the NF-ĸB signaling pathway. The present study indicates that genistein could reverse ox-LDL-induced inflammation through miR-155/SOCS1-mediated repression of the NF-ĸB signaling pathway in HUVECs.
染料木黄酮在动脉粥样硬化的预防中起着重要作用。然而，其潜在机制尚未得到充分研究。在这项研究中，用人脐静脉内皮细胞（HUVEC）预先用染料木黄酮（10、100 和 1000nM）处理 6 小时，然后再用 ox-LDL（50mg/L）处理 24 小时。结果表明，ox-LDL 诱导 E-选择素、P-选择素、单核细胞趋化蛋白-1、白细胞介素-8、血管细胞黏附分子-1 和细胞间黏附分子-1 的表达，而染料木黄酮则拮抗了这些表达。随着染料木黄酮（10、100 和 1000nM）的增加，抑制作用进一步增强。进一步的分析表明，染料木黄酮的作用与降低 miR-155 和升高 SOCS1 有关，miR-155 模拟物或 SOCS1 siRNA 在改善炎症方面作用相似。此外，染料木黄酮的作用伴随着 NF-ĸB 信号通路的抑制。本研究表明，染料木黄酮可以通过 miR-155/SOCS1 介导的 NF-ĸB 信号通路抑制来逆转 ox-LDL 诱导的炎症。
