FOOD SCIENCE ›› 2017, Vol. 38 ›› Issue (13): 174-181.doi: 10.7506/spkx1002-6630-201713029

• Nutrition & Hygiene • Previous Articles     Next Articles

Establishment of Angiotensin Ⅱ-Induced Model in Human Umbilical Vein Endothelial Cells

LIU Guoyan, SUN Beibei, ZHANG Jie, YU Suning, JIANG Donglei, FANG Weiming, XU Xin   

  1. College of Food Science and Engineering, Yangzhou University, Yangzhou 225127, China
  • Online:2017-07-15 Published:2017-07-11

Abstract: Objective: This research was aimed to establish a hypertensive damage model in human umbilical vein endothelial cells (HUVECs) induced by angiotensin (Ang) Ⅱ. Methods: HUVECs were induced with different concentrations (0.01, 0.10, 1.00 and 10.00 μmol/L) of Ang Ⅱ for different times (3, 6, 9, 12 and 24 h), respectively. The injury degree of HUVECs was evaluated by cellular morphology, viability, function, microstructure, and apoptosis. The optimal concentration and time were obtained by using variance analysis and multiple comparison tests. Results: Ang Ⅱ induced injury in HUVECs in a dose- and time-dependent manner. The optimal Ang Ⅱ concentration and induction time were respectively 1.00 μmol/L, and 12 h. After 12 h induction by 1 μmol/L Ang Ⅱ induced, the cell viability was 44.85%, nitric monoxide (NO) content was 43.57 μmol/L, total nitric oxide synthase (TNOS) activity was 6.99 U/mg pro, endothelial nitric oxide synthase (eNOS) activity was 1.89 U/mg pro, malonaldehyde (MDA) content was 7.46 nmol/mL, superoxide dismutase (SOD) activity was 27.29 U/mg pro, and apoptosis percentage was 41.5%. The microstructure showed that the nuclear membrane shrivel and nucleolus disappeared, and a large number of air bubbles appeared inside the cytoplasm. Small and swollen mitochondria, only a small number of expanded rough endoplasmic reticula, partial loss of ribosome, and endoplasmic reticulum expansion were observed, but the cells did not collapse, and still maintained their normal structure. Conclusion: Induction with 1.00 μmol/L Ang Ⅱ for 12 h allows successful establishment of a hypertensive damage model in HUVECs.

Key words: angiotensin Ⅱ (Ang Ⅱ), human umbilical vein endothelial cells (HUVECs), hypertension, cell model

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