Hydroxysafflor Yellow A suppresses thrombin generation and inflammatory responses following focal cerebral ischemia-reperfusion in rats

Bioorg Med Chem Lett. 2010 Jul 15;20(14):4120-4. doi: 10.1016/j.bmcl.2010.05.076. Epub 2010 Jun 11.

Abstract

Hydroxysafflor Yellow A has been demonstrated to attenuate pressure overloaded hypertrophy in rats and inhibit platelet aggregation. Herein we found that Hydroxysafflor Yellow A prevented cerebral ischemia-reperfusion injury by inhibition of thrombin generation. In addition, treatment with Hydroxysafflor Yellow A significantly inhibited NF-kappaB p65 nuclear translation and p65 binding activity, both mRNA and protein levels of ICAM-1 and the infiltration of neutrophils. Mean while, Hydroxysafflor Yellow A had the capacity to improve neurological deficit scores, increase the number of the surviving hippocampal CA1 pyramidal cells and decrease the plasma angiotensin II level. These results illustrated that anti-cerebral ischemic mechanism of Hydroxysafflor Yellow A may be due to its suppression of thrombin generation and inhibition of thrombin-induced inflammatory responses by reducing angiotensin II content.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain Ischemia / metabolism*
  • Brain Ischemia / pathology
  • Chalcone / analogs & derivatives*
  • Chalcone / pharmacology
  • Inflammation / prevention & control*
  • Male
  • Quinones / pharmacology*
  • Rats
  • Rats, Wistar
  • Reperfusion Injury*
  • Thrombin / antagonists & inhibitors*
  • Thrombin / biosynthesis

Substances

  • Quinones
  • hydroxysafflor yellow A
  • Chalcone
  • Thrombin