人参总皂苷通过血管紧张素Ⅱ受体 AT1 亚型抑制血管紧张素Ⅱ诱导的人血管内皮细胞损伤。
Total saponins of panax ginseng inhibiting human endothelium cells' damages induced by angiotensin II via AT1 receptor.
机构信息
Department of Anesthesiology, The Third Hospital Affiliated Xinxiang Medical University, Xinxiang 453003, China.
出版信息
J Ethnopharmacol. 2011 Nov 18;138(2):439-44. doi: 10.1016/j.jep.2011.09.036. Epub 2011 Sep 22.
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-α (TNF-α) 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 30min, before with AT1 receptor antagonist (AT1RA) and TSPG. Tested were NAD(P)H oxidase subunit P22phox mRNA, intracellular reactive oxidative species (ROS), nuclear factor-κB (NF-κB) and vascular cell adhesion molecule-1(VCAM) expression.
RESULTS
In the in vivo study, the plasma TNF-α 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-κB 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.
目的
研究人参总皂苷（TSPG）对血管紧张素 II（AngII）诱导的内皮细胞损伤的作用及机制。
材料与方法
50 只 SD 大鼠随机分为三组：假手术组、AngII 组和 AngII+TSPG 组。AngII 组和 AngII+TSPG 组大鼠背部皮下埋入 AngII 渗透泵，AngII+TSPG 组大鼠通过胃管给予 TSPG。采用酶联免疫吸附试验（ELISA）法检测血浆肿瘤坏死因子-α（TNF-α）和一氧化氮（NO）水平，扫描电子显微镜（SEM）观察人主动脉内皮细胞（HAECs）形态。此外，用 AngII 和 TSPG 或 Ang-（1-7）处理 HAECs，用 AngII 孵育 ECs 30min 后，再用 AT1 受体拮抗剂（AT1RA）和 TSPG 处理。检测 NAD（P）H 氧化酶亚单位 P22phoxmRNA、细胞内活性氧（ROS）、核因子-κB（NF-κB）和血管细胞黏附分子-1（VCAM）的表达。
结果
在体内研究中，与假手术组相比，AngII 组大鼠血浆 TNF-α 显著升高，AngII+TSPG 组显著降低；而 NO 测量结果则相反。AngII 组胸主动脉 EC 表面脱落，AngII+TSPG 组大部分得到恢复。在体外研究中，TSPG 显著降低了 AngII 诱导的 NAD（P）H 氧化酶亚单位 P22phox、NF-κB 和细胞内 ROS 产生的表达，AT1 受体拮抗剂部分阻断了 TSPG 的抑制作用。
结论
TSPG 通过 AT1 受体途径可预防 AngII 诱导的 ECs 损伤。
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