Total saponins of panax ginseng inhibiting human endothelium cells' damages induced by angiotensin II via AT1 receptor

Aim of the study To investigate the effect and mechanism of total saponins of panax ginseng (TSPG) on the damages of endothelium cells induced by Angiotensin II (AngII). Materials and Methods Fifty SD rats were randomly divided into three groups: sham, AngII, and AngII + TSPG. The osmotic pumps with AngII were embedded in the backs of the animals in AngII and AngII + TSPG group, and TSPG was delivered through the gastric tube in AngII + TSPG group. The plasma tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) were measured by ELISA, and Human aortic endothelial cells (HAECs) were observed with scanning electron microscope (SEM). In addition, HAECs were treated with AngII and TSPG or Ang-(1-7), and the ECs were incubated with AngII for 30 min, before with AT1 receptor antagonist (AT1RA) and TSPG. Tested were NAD(P)H oxidase subunit P22phox mRNA, intracellular reactive oxidative species (ROS), nuclear factor-kappa B (NF-kappa B) and vascular cell adhesion molecule-1(VCAM) expression. Results In the in vivo study, the plasma TNF-a increased significantly in AngII group when compared with the sham group, and decreased significantly in AngII + TSPG group. However, NO measurement produced opposite results. The surface of the thoracic aorta ECs desquamated in the AngII group, and most of them were restored in the AngII + TSPG group. In the in vitro study, TSPG reduced significantly the expressions of the NAD(P)H oxidize subunit P22phox, NF-kappa B and intracellular ROS production induced by AngII, and the inhibitory effects of TSPG were partially blocked by AT1 receptor antagonist. Conclusion TSPG was found to be capable of preventing the damages of ECs induced by Ang II via AT1 receptor pathway. (C) 2011 Elsevier Ireland Ltd. All rights reserved.