Inhibition of nuclear translocation of notch intracellular domain (NICD) by diosgenin prevented atherosclerotic disease progression

被引:22
作者
Binesh, Ambika [1 ]
Devaraj, Sivasithambaram Niranjali [2 ]
Devaraj, Halagowder [1 ]
机构
[1] Univ Madras, Sch Life Sci, Dept Zool, Unit Biochem, Guindy Campus, Madras 600025, Tamil Nadu, India
[2] Univ Madras, Sch Life Sci, Dept Biochem, Guindy Campus, Madras 600025, Tamil Nadu, India
关键词
Atherogenic diet; Notch-NICD; Diosgenin; DAPT; Macrophage differentiation; IN-VIVO; MACROPHAGE ACTIVATION; ATHEROGENIC DIET; VASCULAR INJURY; LIVER; INFLAMMATION; PLASMA; CELLS; RATS; LIPOPROTEINS;
D O I
10.1016/j.biochi.2018.02.011
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Notch signaling plays a pivotal role in homeostasis and cardiovascular development. The role of notch signaling in atherosclerosis cannot be complete without analysing the key role of notch in macrophages, which trigger the inflammatory response and subsequent plaque formation in atherosclerosis. Diosgenin showed its anti-atherosclerotic property by the unifying mechanism of suppressing the expression of notch signaling pathway, particularly the nuclear translocation of notch intracellular domain (NICD) in aorta and in differentiated macrophage cells. It is further confirmed by the inhibition of NICD by DAPT (N-[N-(3, 5-difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butyl ester), which also restricted the differentiation of macrophage. Hence, inhibition of nuclear translocation of NICD by diosgenin aids in preventing atherosclerosis. (c) 2018 Published by Elsevier B.V.
引用
收藏
页码:63 / 71
页数:9
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