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.

Notch信号在体内平衡和心血管发育中起关键作用。如果不分析缺口在巨噬细胞中的关键作用，缺口信号在动脉粥样硬化中的作用就无法完成，而巨噬细胞会触发炎症反应并随后在动脉粥样硬化中形成斑块。薯os皂苷元通过抑制Notch信号通路表达的统一机制显示出其抗动脉粥样硬化特性，特别是在主动脉和分化的巨噬细胞中，Notch细胞内结构域（NICD）的核易位。通过DAPT（N- [N-（3，5-二氟苯乙酰基）-1-丙氨酰基] -S-苯基甘氨酸t抑制NICD进一步证实了这一点。-丁酯），这也限制了巨噬细胞的分化。因此，薯di皂苷元抑制NICD的核易位有助于预防动脉粥样硬化。