Hydroxysafflor Yellow A suppresses thrombin generation and inflammatory responses following focal cerebral ischemia-reperfusion in rats.
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.
Sun
Xia
X
Department of Pharmacology, School of Medicine, Shandong University, 44#, Wenhua Xi Road, Jinan 250012, PR China.
Wei
Xinbing
X
Qu
Sifeng
S
Zhao
Yunxue
Y
Zhang
Xiumei
X
D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology; D002599:Chalcone / Q000031:analogs & derivatives* / Q000494:pharmacology; D007249:Inflammation / Q000517:prevention & control*; D008297:Male; D011809:Quinones / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury; D013917:Thrombin / Q000037:antagonists & inhibitors* / Q000096:biosynthesis
D011809:Quinones; C085278:hydroxysafflor yellow A; D002599:Chalcone; D013917:Thrombin