Cao Yongwen, Zheng Lulu, Liu Shao, Peng Zhenyu, Zhang Saidan
Department of Cardiology, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China.
Department of Pharmacology, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China.
Exp Ther Med. 2014 May;7(5):1187-1192. doi: 10.3892/etm.2014.1554. Epub 2014 Feb 17.
Angiotensin II (Ang II) is a neuroendocrine factor that promotes hypertension and has been implicated in vascular inflammation through the induction of reactive oxygen species (ROS) and proinflammatory genes in endothelial cells. However, relatively little attention has been paid to the effect of Ang II on fractalkine (FKN), an important chemokine involved in endothelial dysfunction. In the study, we aimed to investigate the protective role of total flavonoids from Plumula Nelumbinis (TFPN), the main component extracted from Semen Nelumbinis, in Ang II-induced oxidative stress injury in human umbilical vein endothelial cells (HUVECs). Furthermore, we studied whether TFPN could attenuate the Ang II-induced generation of ROS and the activation of nuclear factor-κB (NF-κB); whether these Ang II-induced effects were inhibited by apocynin (a nicotinamide adenine dinucleotide phosphate oxidase inhibitor) and pyrrolidine dithiocarbamate (an NF-κB inhibitor). In the present study, it was observed that total flavonoids from Plumula Nelumbinis (TFPN), the main component extracted from Semen Nelumbinis, concentration-dependently inhibited the FKN production induced by Ang II in human umbilical vein endothelial cells (HUVECs). Furthermore, TFPN attenuated the Ang II-induced generation of ROS and the activation of nuclear factor-κB (NF-κB); these Ang II-induced effects were also inhibited by apocynin (a nicotinamide adenine dinucleotide phosphate oxidase inhibitor) and pyrrolidine dithiocarbamate (an NF-κB inhibitor). In conclusion, the findings of the present study indicate that TFPN attenuate Ang II-induced upregulation of FKN by inhibiting the ROS/NF-κB pathway in HUVECs and thus have a suppressive effect on vascular inflammation.
血管紧张素 II（Ang II）是一种促进高血压的神经内分泌因子，通过在内皮细胞中诱导活性氧（ROS）和促炎基因参与血管炎症反应。然而，Ang II 对趋化因子（FKN）的影响相对较少受到关注，FKN 是一种参与内皮功能障碍的重要趋化因子。在本研究中，我们旨在探讨莲子心总黄酮（TFPN），即从莲子中提取的主要成分，对 Ang II 诱导的人脐静脉内皮细胞（HUVECs）氧化应激损伤的保护作用。此外，我们研究了 TFPN 是否能减轻 Ang II 诱导的 ROS 生成和核因子κB（NF-κB）的激活；这些 Ang II 诱导的效应是否被阿朴吗啡（一种烟酰胺腺嘌呤二核苷酸磷酸氧化酶抑制剂）和吡咯烷二硫代氨基甲酸盐（一种 NF-κB 抑制剂）所抑制。在本研究中，观察到莲子心总黄酮（TFPN），即从莲子中提取的主要成分，浓度依赖性地抑制 Ang II 诱导的人脐静脉内皮细胞（HUVECs）中 FKN 的产生。此外，TFPN 减轻了 Ang II 诱导的 ROS 生成和核因子κB（NF-κB）的激活；这些 Ang II 诱导的效应也被阿朴吗啡（一种烟酰胺腺嘌呤二核苷酸磷酸氧化酶抑制剂）和吡咯烷二硫代氨基甲酸盐（一种 NF-κB 抑制剂）所抑制。总之，本研究结果表明，TFPN 通过抑制 HUVECs 中的 ROS/NF-κB 途径减轻 Ang II 诱导的 FKN 上调，从而对血管炎症具有抑制作用。
