TY  - JOUR
T1  - Amygdalin Attenuates Atherosclerosis Progress Through Inhibiting of Toll-Like Receptors Expression and Activity
AU - Zhao, Fei AU - Yang, Zhirong 
JO  - Journal of Animal and Veterinary Advances
VL  - 11
IS  - 10
SP  - 1613
EP  - 1621
PY  - 2012
DA  - 2001/08/19
SN  - 1680-5593
DO  - javaa.2012.1613.1621
UR  - https://makhillpublications.co/view-article.php?doi=javaa.2012.1613.1621
KW  - Amygdalin
KW  -Toll-Like Receptor (TLR)
KW  -MyD88-dependent signaling
KW  -atherosclerosis
KW  - mice
KW  -protien
AB  - Toll-Like Receptors (TLRs) and TLR signaling cascade play a pivotal role in the innate immune responses, especially in initiation and progression of atherosclerosis. Thus in the present study, researchers examined the anti-atherosclerosis effects of amygdalin and explored whether the anti-atherosclerosis function was achieved via inhibiting TLRs expression and TLR signaling. ApoE knockout mice were fed on high fat diet and received daily injection of amygdalin. By comparing lipid profiles, atherosclerotic lesions and serum proinflammatory cytokine concentrations, mice untreated with amygdalin experienced more severe atherosclerosis compared with mice received amygdalin treatment. TLR2 and TLR4 mRNA and protein levels were found to be reduced after amygdalin treatment. Expression of key MyD88-dependent signaling components was inhibited by amygdalin. Amygdalin may play a protective role in the development of atherosclerosis via the inhibition of TLR2 and TLR4 expression.
ER  - 