Preprint / Version 1

Ayurvedic preparations of Raudra Rasa inhibit agonist‐mediated platelet activation and restrict thrombogenicity without affecting cell viability

Authors

  • Susheel Chaurasia Center for Advanced Research on Platelet Signaling and Thrombosis Biology, Department of Biochemistry, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India
  • Vipin Singh Center for Advanced Research on Platelet Signaling and Thrombosis Biology, Department of Biochemistry, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India
  • Mohammad Ekhlak Center for Advanced Research on Platelet Signaling and Thrombosis Biology, Department of Biochemistry, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India
  • Manoj Dash Department of Rasa Shastra & B Kalpana, Government Ayurved College, Raipur, India
  • Namrata Joshi Department of Rasa Shastra, Faculty of Ayurveda, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India
  • Debabrata Dash Center for Advanced Research on Platelet Signaling and Thrombosis Biology, Department of Biochemistry, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India

Keywords:

AKT, CRR, mROS, MRR, platelets, RRE

Abstract

Ayurveda is considered to be one of the most ancient forms of medicine still practiced. The Ayurvedic preparation Raudra Rasa and its derivatives have been widely employed against cancer since the 12th century, but the effect of these traditional formulations on platelet function and signaling has not previously been examined. Here we demonstrate that Raudra Rasa and its derivatives significantly reduce thrombin‐induced integrin activation and granule secretion in platelets, as observed by reduced PAC‐1 binding and P‐selectin externalization, respectively. These formulations also inhibited thrombin‐stimulated phosphatidylserine exposure, mitochondrial reactive oxygen species generation, and mitochondrial transmembrane potential in platelets. Consistent with the above, Raudra Rasa significantly reduced thrombin‐induced tyrosine phosphorylation of the platelet proteins, as well as phosphorylation of the enzymes AKT and GSK‐3β. In summary, Raudra Rasa inhibits agonist‐mediated platelet activation without affecting cell viability, suggesting it may have therapeutic potential as an anti‐platelet/anti‐thrombotic agent. Keywords: AKT, CRR, mROS, MRR, platelets, RRE

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