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Liu D, Pei D, Hu H, et al. Effects and Mechanisms of Vitamin C Post-Conditioning on Platelet Activation after Hypoxia/Reoxygenation. Transfus Med Hemother. 2019;47(2):110-118doi: 10.1159/000500492.
Liu, D., Pei, D., Hu, H., Gu, G., & Cui, W. (2020). Effects and Mechanisms of Vitamin C Post-Conditioning on Platelet Activation after Hypoxia/Reoxygenation. Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie, 47(2), 110-118. https://doi.org/10.1159/000500492
Liu, Demin, et al. "Effects and Mechanisms of Vitamin C Post-Conditioning on Platelet Activation after Hypoxia/Reoxygenation." Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie vol. 47,2 (2020): 110-118. doi: https://doi.org/10.1159/000500492
Liu D, Pei D, Hu H, Gu G, Cui W. Effects and Mechanisms of Vitamin C Post-Conditioning on Platelet Activation after Hypoxia/Reoxygenation. Transfus Med Hemother. 2020 Apr;47(2):110-118. doi: 10.1159/000500492. Epub 2019 May 28. PMID: 32355470; PMCID: PMC7184846.
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Transfus Med Hemother. 2020 Apr;47(2):110-118. doi: 10.1159/000500492. Epub 2019 May 28.

Effects and Mechanisms of Vitamin C Post-Conditioning on Platelet Activation after Hypoxia/Reoxygenation.

Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie

Demin Liu, Dongguo Pei, Haijuan Hu, Guoqiang Gu, Wei Cui

Affiliations

  1. Department of Cardiology, Second Hospital of Hebei Medical University, Shijiazhuang, China.

PMID: 32355470 PMCID: PMC7184846 DOI: 10.1159/000500492

Abstract

BACKGROUND: Platelet activation occurs upon ischemia/reperfusion and is related to the generation of reactive oxygen species (ROS) during this process. Vitamin C (VC) is a powerful antioxidant. VC scavenges ROS, reduces platelet activation, and attenuates reperfusion injury. However, the effects of VC on platelets undergoing hypoxia/reoxygenation (H/R) remain unclear.

OBJECTIVES: Herein, we evaluated the effects of VC on platelets in vitro following H/R and the related mechanisms.

METHOD: Fresh platelets were collected from 67 volunteers at the Blood Center of Hebei Province. Platelets were diluted with saline to a concentration of 2.00 × 1011/L. Aggregation and the curve slope were evaluated within 4 h with a whole-blood impedance analyzer. To determine the optimal experimental time, platelets were treated with hypoxia or reoxygenation for different times, and impedance aggregometry was carried out by measuring changes in electrical impedance induced by arachidonic acid (0.5 mM) and adenosine diphosphate (10 µM), thereby establishing the H/R model. Three antioxidants (VC, melatonin, and probucol) were used to treat platelets after H/R, and impedance aggregometry was used to determine their effects on platelet aggregation. The influence of VC on apoptosis-related indicators was detected. ROS and the mitochondrial membrane potential were observed by inverted fluorescence microscopy and flow cytometry, respectively. Related protein levels were detected by Western blotting.

RESULTS: ROS scavengers inhibited platelet activation and aggregation in a concentration-dependent manner. VC post-conditioning scavenged ROS, downregulated cytochrome C, Bax, and caspase-9 proteins, and upregulated Bcl-2 protein. These effects collectively blocked platelet apoptosis and inhibited platelet aggregation.

CONCLUSIONS: VC inhibited platelet aggregation by blocking apoptosis. Thus, VC may have applications in the treatment of platelet-related diseases.

Copyright © 2019 by S. Karger AG, Basel.

Keywords: Apoptosis; Platelet aggregation; Platelets; Reactive oxygen species; Vitamin C

Conflict of interest statement

The authors have no conflicts of interest to declare.

References

  1. Tohoku J Exp Med. 2011;225(1):23-34 - PubMed
  2. Transfus Apher Sci. 2003 Jun;28(3):285-95 - PubMed
  3. J Thromb Haemost. 2008 Oct;6(10):1780-8 - PubMed
  4. Life Sci. 2016 Nov 15;165:43-55 - PubMed
  5. Cardiovasc Ther. 2011 Dec;29(6):385-94 - PubMed
  6. J Thromb Haemost. 2006 Dec;4(12):2656-63 - PubMed
  7. Annu Rev Physiol. 2008;70:73-91 - PubMed
  8. FEBS Lett. 2011 Jul 21;585(14):2345-51 - PubMed
  9. J Thromb Thrombolysis. 2012 May;33(4):397-411 - PubMed
  10. Cardiovasc Res. 2004 Feb 15;61(3):498-511 - PubMed
  11. Arterioscler Thromb Vasc Biol. 2011 Aug;31(8):1766-71 - PubMed
  12. Thromb Res. 2002 Apr 15;106(2):143-8 - PubMed
  13. J Cardiovasc Pharmacol Ther. 2017 Mar;22(2):122-132 - PubMed
  14. Mol Cell Biochem. 2013 Jan;373(1-2):73-83 - PubMed
  15. Am J Physiol Heart Circ Physiol. 2006 Feb;290(2):H692-9 - PubMed
  16. Curr Neuropharmacol. 2017 Apr;15(3):434-443 - PubMed
  17. Blood. 2002 Aug 1;100(3):917-24 - PubMed
  18. Arterioscler Thromb Vasc Biol. 2011 Jan;31(1):15-26 - PubMed
  19. Circulation. 1997 Feb 18;95(4):787-9 - PubMed
  20. J Thromb Haemost. 2003 Jan;1(1):171-7 - PubMed
  21. Biochem Biophys Res Commun. 2004 Jul 23;320(2):303-10 - PubMed
  22. Sci Rep. 2016 Dec 02;6:38161 - PubMed
  23. Platelets. 2002 May;13(3):175-82 - PubMed
  24. Free Radic Biol Med. 1997;22(6):999-1006 - PubMed
  25. Platelets. 2016 Sep;27(6):497-504 - PubMed
  26. Prostaglandins Leukot Med. 1987 Sep;29(1):49-59 - PubMed
  27. Circulation. 2000 Feb 29;101(8):841-3 - PubMed
  28. Thromb Haemost. 2000 Mar;83(3):485-90 - PubMed
  29. Zhonghua Xue Ye Xue Za Zhi. 2014 Jun;35(6):511-4 - PubMed
  30. Arterioscler Thromb Vasc Biol. 2016 May;36(5):846-54 - PubMed
  31. Antioxid Redox Signal. 2012 Nov 15;17(10):1447-85 - PubMed

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