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Astragalus polysaccharide ameliorates H2O2-induced human umbilical vein endothelial cell injury

  • Authors:
    • Ronghui Han
    • Futian Tang
    • Meili Lu
    • Chonghua Xu
    • Jin Hu
    • Meng Mei
    • Hongxin Wang
  • View Affiliations / Copyright

    Affiliations: Key Laboratory of Cardiovascular and Cerebrovascular Drug Research of Liaoning Province, Drug Research Institute, Jinzhou Medical University, Jinzhou, Liaoning 121001, P.R. China, Department of Pharmacology, Key Laboratory of Cardiovascular and Cerebrovascular Drug Research of Liaoning Drug Research Institute, Jinzhou Medical University, Jinzhou, Liaoning 121001, P.R. China
    Copyright: © Han et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 4027-4034
    |
    Published online on: April 26, 2017
       https://doi.org/10.3892/mmr.2017.6515
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Abstract

Endothelial dysfunction caused by reactive oxygen species (ROS) has been implicated in numerous cardiovascular diseases. Astragalus polysaccharide (APS), an important bioactive component extracted from the Chinese herb Astragalus membranaceus, has been widely used for the treatment of cardiovascular disease. The present study aimed to investigate the effects of APS on hydrogen peroxide (H2O2)‑induced human umbilical vein endothelial cell (HUVEC) injury. Following treatment with 400 µM H2O2 for 24 h, cell viability was decreased and apoptosis was increased. However, pretreatment with APS for 1 h significantly attenuated H2O2‑induced injury in HUVECs. In addition, APS decreased intracellular ROS levels, increased the protein expression of endothelial nitric oxide synthase and copper‑zinc superoxide dismutase, elevated intracellular cyclic guanosine monophosphate (an activity marker for nitric oxide) levels and restored the mitochondrial membrane potential, compared with cells treated with H2O2 only. In conclusion, the results of the present study suggested that APS may protect HUVECs from injury induced by H2O2 via increasing the cell antioxidant capacity and nitric oxide (NO) bioavailability, which may contribute to the improvement of the imbalance between ROS and NO levels.
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Copy and paste a formatted citation
Spandidos Publications style
Han R, Tang F, Lu M, Xu C, Hu J, Mei M and Wang H: Astragalus polysaccharide ameliorates H2O2-induced human umbilical vein endothelial cell injury. Mol Med Rep 15: 4027-4034, 2017.
APA
Han, R., Tang, F., Lu, M., Xu, C., Hu, J., Mei, M., & Wang, H. (2017). Astragalus polysaccharide ameliorates H2O2-induced human umbilical vein endothelial cell injury. Molecular Medicine Reports, 15, 4027-4034. https://doi.org/10.3892/mmr.2017.6515
MLA
Han, R., Tang, F., Lu, M., Xu, C., Hu, J., Mei, M., Wang, H."Astragalus polysaccharide ameliorates H2O2-induced human umbilical vein endothelial cell injury". Molecular Medicine Reports 15.6 (2017): 4027-4034.
Chicago
Han, R., Tang, F., Lu, M., Xu, C., Hu, J., Mei, M., Wang, H."Astragalus polysaccharide ameliorates H2O2-induced human umbilical vein endothelial cell injury". Molecular Medicine Reports 15, no. 6 (2017): 4027-4034. https://doi.org/10.3892/mmr.2017.6515
Copy and paste a formatted citation
x
Spandidos Publications style
Han R, Tang F, Lu M, Xu C, Hu J, Mei M and Wang H: Astragalus polysaccharide ameliorates H2O2-induced human umbilical vein endothelial cell injury. Mol Med Rep 15: 4027-4034, 2017.
APA
Han, R., Tang, F., Lu, M., Xu, C., Hu, J., Mei, M., & Wang, H. (2017). Astragalus polysaccharide ameliorates H2O2-induced human umbilical vein endothelial cell injury. Molecular Medicine Reports, 15, 4027-4034. https://doi.org/10.3892/mmr.2017.6515
MLA
Han, R., Tang, F., Lu, M., Xu, C., Hu, J., Mei, M., Wang, H."Astragalus polysaccharide ameliorates H2O2-induced human umbilical vein endothelial cell injury". Molecular Medicine Reports 15.6 (2017): 4027-4034.
Chicago
Han, R., Tang, F., Lu, M., Xu, C., Hu, J., Mei, M., Wang, H."Astragalus polysaccharide ameliorates H2O2-induced human umbilical vein endothelial cell injury". Molecular Medicine Reports 15, no. 6 (2017): 4027-4034. https://doi.org/10.3892/mmr.2017.6515
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