Title of article :
The Anti-Atherosclerotic Effect of Prosopis Farcta is Associated with the Inhibition of VCAM-1 and ICAM-1
Author/Authors :
Bahrami, Gholamreza Medical Biology Research Center - Kermanshah University of Medical Sciences, Kermanshah, Iran , Hosseinzadeh, Leila Pharmaceutical Sciences Research Center - Faculty of Pharmacy - Kermanshah University of Medical Sciences, Kermanshah, Iran , Azadid, Zahra Students research committee - Faculty of Pharmacy - Kermanshah University of Medical Sciences, Kermanshah, Iran , Mohammadi, Bahareh Medical Biology Research Center - Kermanshah University of Medical Sciences, Kermanshah, Iran , Mahdiyan, Zahra Students research committee - Faculty of Pharmacy - Kermanshah University of Medical Sciences, Kermanshah, Iran , Hajialyani, Marziyeh Pharmaceutical Sciences Research Center - Faculty of Pharmacy - Kermanshah University of Medical Sciences, Kermanshah, Iran , Farzaei, Mohammad Hosein School of Pharmacy - Kermanshah University of Medical Sciences, Kermanshah, Iran
Pages :
11
From page :
357
To page :
367
Abstract :
This study evaluated the anti-atherosclerosis effect of aqueous extract and polysaccharide-enriched fraction of Prosopis farcta on adhesion and inflammatory cascades in vascular endothelial cells and related molecular mechanisms. Cellular toxicities of LPS, plant extract and polysaccharide-enriched fraction were analyzed in vitro using the MTT method. The ROS accumulation, mRNA expression of ICAM1 and VCAM1, and COX activity were measured in HUVEC cells. These results revealed a new underlying mechanism for anti-atherosclerosis effect of P. farcta and polysaccharide-enriched fraction by attenuating inflammatory cascade mediated by COX expression, modulating expression of celladhesion molecules including VCAM-1 and ICAM-1, and diminishing oxidative stress agents.
Keywords :
Prosopis Farcta , LPS , HUVEC , Cytotoxicity , Adhesion Molecules , Atherosclerosis
Journal title :
Journal of Reports in Pharmaceutical Sciences
Serial Year :
2018
Record number :
2524693
Link To Document :
بازگشت