Salvianolic acid A inhibits angiotensin II-induced proliferation of human umbilical vein endothelial cells by attenuating the production of ROS

• Published in: Acta pharmacologica Sinica Vol. 33; no. 1; pp. 41 - 48
• Main Authors: Yang, Luan-luan, Li, Dong-ye, Zhang, Yan-bin, Zhu, Man-yi, Chen, Dan, Xu, Tong-da
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.01.2012; Nature Publishing Group
• Subjects: Angiotensin II - pharmacology; Biomedical and Life Sciences; Biomedicine; Caffeic Acids - chemistry; Caffeic Acids - pharmacology; Cell Proliferation - drug effects; Human Umbilical Vein Endothelial Cells - cytology; Human Umbilical Vein Endothelial Cells - drug effects; Human Umbilical Vein Endothelial Cells - physiology; Humans; Immunology; Internal Medicine; Lactates - chemistry; Lactates - pharmacology; Medical Microbiology; Molecular Structure; NADPH Oxidase 4; NADPH Oxidases - metabolism; Original; original-article; Pharmacology/Toxicology; Phosphorylation; Proto-Oncogene Proteins c-akt - metabolism; Reactive Oxygen Species - metabolism; Signal Transduction - drug effects; Vaccine; 人脐静脉内皮细胞; 扩散; 活性氧; 生产; 血管内皮细胞; 血管紧张素; 诱导; 酚酸; phospho-Akt; angiotensin II; human umbilical vein endothelial cells; ROS; salvianolic acid A; phospho-Src; NADPH oxidase 4
• ISSN: 1671-4083; 1745-7254
• DOI: 10.1038/aps.2011.133

Aim： To investigate the action of salvianolic acid A （SalA） on angiotensin II （Ang II）-induced proliferation of human umbilical vein endothelial cells （HUVECs） and the possible signaling pathways mediating this action. Methods： Cell proliferation was examined with MTT assay. The expression levels of Src phosphorylation （phospho-Src）, Akt phospho- rylation （phospho-Akt）, and NADPH oxidase 4 （Nox4） in HUVECs were determined by Western blot. The production of reactive oxygen species （ROS） was estimated using fluorescence-activated cell sorting （FACS）. Results： SalA （6.25-50 pmol/L） did not affect the viability of HUVECs. Treatment of HUVECs with Ang II （1 pmol/L） markedly increased the cell viability; pretreatment of HUVECs with SalA （12.5, 25, and 50 pmol/L） prevented Ang II-induced increase of the cell viability in a concentration-dependent manner. Treatment of HUVECs with Ang II （1 IJmol/L） markedly up-regulated the protein expression levels of phospho-Src, phospho-Akt （473） and Nox4; pretreatment of HUVECs with SalA （12.5, 25, and 50 pmol/L） blocked all the effects in a concentration-dependent manner. Treatment of HUVECs with Ang II （1 pmol/L） dramatically increased ROS production in HUVECs; pre- treatment of HUVECs with SalA （12.5, 25, and 50 pmol/L） blocked the ROS production in a concentration-dependent manner. Conclusion： SalA inhibits Ang II-induced proliferation of HUVECs via reducing the expression levels of phospho-Src and phospho-Akt （473）, thereby attenuating the production of ROS.