Hydroxysafflor Yellow A Attenuates Hydrogen Peroxide-Induced Oxidative Damage on Human Umbilical Vein Endothelial Cells.

Yuefeng Xie,Miaomiao Xue,Zhaoyue Fan,Chengxian Gao,Bo Jin,Yan Guo,Shidong Cao,Elia Ranzato

doi:10.1155/2020/8214128

Abstract

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 H2O2 and to provide a theoretical basis for the clinical treatment of cardiovascular diseases related to traditional Chinese medicine. Based on the establishment of an H2O2-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 H2O2-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 H2O2-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.

Highlights

Vascular endothelial cells are monolayer of cells located between plasma and vascular tissue, which has emerged as the key regulator of vascular homeostasis [1]
Oxidative stress is caused by an imbalance between oxidative and antioxidant mechanisms in the body [7], and excessive accumulation of intracellular redox products has various toxic effects on cells, leading to the occurrence of related diseases [8]. erefore, endothelial dysfunction caused by oxidative stress is an important factor, leading to vascular damage in metabolism and cardiovascular diseases, and suppression of oxidative stress is considered as a potential strategy for CVD [9, 10]
E data showed that the cell viability after treatment with Hydroxysafflor yellow A (HSYA) at a concentration of 0.5–10 μg/ml was improved to varying degrees compared with the H2O2 model group (Figure 2(b)). erefore, in all subsequent experiments, the two most significant concentrations of 8 μg/ml and 4 μg/ml were used

Summary

Introduction

Vascular endothelial cells are monolayer of cells located between plasma and vascular tissue, which has emerged as the key regulator of vascular homeostasis [1]. Us, restoring impaired vascular homeostasis by improving endothelial function can be a promising therapeutic target in the treatment of various CVDs [5]. Several studies have shown that oxidative stress is a vital cause of endothelial dysfunction [6]. Oxidative stress is caused by an imbalance between oxidative and antioxidant mechanisms in the body [7], and excessive accumulation of intracellular redox products has various toxic effects on cells, leading to the occurrence of related diseases [8]. Erefore, endothelial dysfunction caused by oxidative stress is an important factor, leading to vascular damage in metabolism and cardiovascular diseases, and suppression of oxidative stress is considered as a potential strategy for CVD [9, 10]. Studies have shown that HSYA (C27H32O16, MW: 612) has antiinflammatory, antioxidative, and antiangiogenic functions

Methods

Results

Conclusion