Xie Yuefeng, Guo Yan, Cao ShiDong, Xue Miaomiao, Fan ZhaoYue, Gao ChengXian, Jin Bo
College of Life Science, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310053, China.
College of Basic Medicine & Public Health, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310053, China.
Evid Based Complement Alternat Med. 2020 Nov 4;2020:8214128. doi: 10.1155/2020/8214128. eCollection 2020.
Oxidative stress of endothelial cells is thought to be a principal cause that induces many cardiovascular diseases. Hydroxysafflor yellow A (HSYA) is a major active component in traditional Chinese medicine safflower and has been used to cure ischemic cardiovascular diseases in China for many years. This study aims to investigate whether HSYA has a repairing effect on oxidative damage of human umbilical vein endothelial cells (HUVECs) induced by HO and to provide a theoretical basis for the clinical treatment of cardiovascular diseases related to traditional Chinese medicine. Based on the establishment of an HO-induced HUVEC oxidative injury model, the cell viability and proliferation rate were measured by the MTT assay and EdU staining. The intracellular GSH/GSSG ratio and SOD activity were determined by kits. The ROS level was detected by flow cytometry. And the BAX, Bcl-2, PTEN, and AKT expressions were evaluated with western blotting methods. The results showed that HSYA treatment significantly attenuated the HO-induced HUVEC cell damage, increased the intracellular GSH/GSSG ratio and unit SOD activity also, and decreased the intracellular ROS levels. Furthermore, HSYA increased the expressions of AKT and Bcl-2 proteins and inhibited the expressions of BAX and PTEN proteins. These suggest that HSYA exerts repair effects on HO-induced oxidative damage in HUVECs, and the mechanisms may be related to the influence of BAX/Bcl-2 expression and AKT/PTEN signal pathway expression.
内皮细胞的氧化应激被认为是诱发多种心血管疾病的主要原因。羟基红花黄色素A(HSYA)是中药红花中的主要活性成分,多年来在中国一直用于治疗缺血性心血管疾病。本研究旨在探讨HSYA对HO诱导的人脐静脉内皮细胞(HUVECs)氧化损伤是否具有修复作用,为中医药治疗相关心血管疾病提供理论依据。基于建立的HO诱导的HUVEC氧化损伤模型,通过MTT法和EdU染色检测细胞活力和增殖率。采用试剂盒测定细胞内GSH/GSSG比值和SOD活性。通过流式细胞术检测ROS水平。并用蛋白质印迹法评估BAX、Bcl-2、PTEN和AKT的表达。结果表明,HSYA处理可显著减轻HO诱导的HUVEC细胞损伤,增加细胞内GSH/GSSG比值和单位SOD活性,降低细胞内ROS水平。此外,HSYA增加了AKT和Bcl-2蛋白的表达,抑制了BAX和PTEN蛋白的表达。这些表明HSYA对HO诱导的HUVEC氧化损伤具有修复作用,其机制可能与BAX/Bcl-2表达及AKT/PTEN信号通路表达的影响有关。