Study on acting mechanism of extracts from ginseng, notoginseng and chuanxiong for delaying the aging of endothelial cells induced by angiotensin II / 中国中西医结合杂志

ABSTRACT

<p><b>OBJECTIVE</b>To explore the effects of extracts from ginseng, notoginseng and chuanxiong (Ext) on the angiotensin II induced aging of human umbilical endothelial cells (HUVECs) in vitro.</p><p><b>METHODS</b>Cultured HUVECs were divided into 5 groups, the blank control group (A), the model group (B), and the three intervening groups (C, D and E). Except those in Group A, all cells were induced into aging model cells by Ang II in a final concentration of 10(-6) mol/L, and to the three intervening groups, corresponding treatments with low dose Ext (C), high dose Ext (D) and valsartan (E) were accessed. Changes of aging in HUVECs were observed by SA-beta-gal staining; cell cycle was analyzed by flow cytometry; contents of reactive oxygen species (ROS) in cells was measured by laser confocal microscopy; levels of nitric oxide (NO) and anti-superoxide anion in culture medium were examined by nitrate reductase method; and the protein expression of NAD (P) H oxidase p47phox, as well as the angiotensin type 1 and 2 receptor (AT1 R, AT2R) were detected by Western blot.</p><p><b>RESULTS</b>Compared with Group A, in Group B, the positive beta-gal stained HUVECs increased and stagnated at G0-G1 phase, with the fluorescence intensity of ROS evidently enhanced; in the culture medium content of NO and anti-superoxide anion were lowered, and protein expression of p47phox and AT1 R up-regulated. While these aging figures were improved in Group C and D. After intervention with high or low dose of Ext, beta-gal stained HUVECs decreased showing less cells in G0-G1 phase and more cells in G2-M phase, the fluorescence intensity of ROS reduced, contents of NO and anti-superoxide anion increased, and the protein expression of p47phox and AT1 R down-regulated.</p><p><b>CONCLUSION</b>Ext could delay the aging of HUVECs induced by angiotensin II, it is possibly by way of down-regulating the expression of NAD (P) H oxidase subunit-p47phox through AT1 R, and further reducing the superoxide anion production.</p>