褐藻糖胶
TFEB
自噬
细胞生物学
下调和上调
泡沫电池
溶酶体
化学
脂滴
细胞凋亡
生物
生物化学
多糖
胆固醇
脂蛋白
基因
酶
作者
Jiarui Zhao,Bo Hu,Xiao Han,Qiong Yang,Qi Cao,Xia Li,Qian Zhang,Aiguo Ji,Shuliang Song
标识
DOI:10.1016/j.carbpol.2021.118247
摘要
Atherosclerotic cardiovascular disease became one of the major causes of morbidity and mortality worldwide. As a sulfated polysaccharide with anti-inflammatory and hypolipidemic activities, fucoidan can induce autophagy. We show here that fucoidan reduces lipid accumulation in foam cells, which is one of the causes of atherosclerosis. Further studies show that fucoidan promotes autophagy showed by the expression of p62/SQSTM1 and microtubule-associated protein light chain 3 (LC3) II, which can be blocked by autophagy inhibitors 3-MA and bafilomycin A1. In addition, the expression of transcription factor EB (TFEB), master regulator of autophagy and lysosome function, is upregulated after the treatment with fucoidan. Moreover, the knockout of TFEB with small interfering RNA suppressed the effect of fucoidan. Together, fucoidan reduces lipid accumulation in foam cells by enhancing autophagy through the upregulation of TFEB. In view of the role of foam cells in atherosclerosis, fucoidan can be valuable for the treatment of atherosclerosis.
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