Effect of safflor yellow B on vascular endothelial cells injury induced by angiotensin-II.
- Author:
Chao-Yun WANG
1
;
Shu-Ping ZHANG
;
Yong XU
;
Ming YANG
;
Wen-Guo JIANG
;
Hai-Yun LUAN
Author Information
1. School of Pharmacy, Binzhou Medical University, Yantai 264003, China. ytwcy@163.com
- Publication Type:Journal Article
- MeSH:
Angiotensin II;
adverse effects;
Antioxidants;
isolation & purification;
pharmacology;
Apoptosis;
drug effects;
Calcium;
metabolism;
Carthamus tinctorius;
chemistry;
Caspase 3;
metabolism;
Cells, Cultured;
Chalcone;
analogs & derivatives;
isolation & purification;
pharmacology;
Drugs, Chinese Herbal;
isolation & purification;
pharmacology;
Electron Transport Complex IV;
metabolism;
Endothelial Cells;
cytology;
metabolism;
Humans;
Membrane Potential, Mitochondrial;
drug effects;
Mitochondrial Proton-Translocating ATPases;
metabolism;
Plants, Medicinal;
chemistry;
Reactive Oxygen Species;
metabolism;
Vasoconstrictor Agents;
adverse effects
- From:
Acta Pharmaceutica Sinica
2012;47(6):811-815
- CountryChina
- Language:Chinese
-
Abstract:
This study is to investigate protective effect of safflor yellow B (SYB) against vascular endothelial cells (VECs) injury induced by angiotensin-II (Ang-II). VECs were cultured and divided into six groups: control group, Ang-II group, Ang-II + SYB (1 micromolL(-1)) group, Ang-II + SYB (10 micromolL(-1)) group, Ang-II + SYB (100 micromolL(-1)) group and Ang- II + verapamil (10 micromolL(-1)) group. Except control group, all of VECs in other groups were treated with Ang- II at the final concentration of 0.1 micromolL(-1). Mitochondria membrane potential (MMP) and free calcium concentration ([Ca2+]i) were measured by laser scanning confocal microscopy, and mitochondria complex IV activity was detected by BCA method. The levels of reactive oxygen species (ROS) in VECs were analyzed by fluorescence detector and apoptosis of VECs was observed by flow cytometer. Caspase 3 was determined by Western blotting method. Comparing with control group, Ang-II was able to increase [Ca2+]i and ROS level, decrease MMP level, inhibit complex IV activity and enhance caspase 3 activity in VECs, as a result, enhance apoptosis of VECs. But SYB could significantly reduce the result induced by Ang- II relying on different dosages (P < 0.05 or P < 0.01). SYB was able to eliminate the effect of Ang-II on VECs via regulating [Ca2+]i, mitochondrial structure and function and inhibiting apoptosis.
