ABCA1
黄芩苷
ABCG1公司
泡沫电池
肝X受体
过氧化物酶体增殖物激活受体
化学
药理学
炎症
胆固醇
细胞生物学
脂蛋白
内分泌学
内科学
受体
生物
生物化学
核受体
医学
转录因子
运输机
高效液相色谱法
色谱法
基因
作者
Xiayun He,Dan Yu,Weiling Li,Zhou Zheng,Chen-Ling Lv,Cai Li,Peng Liu,Chun-Qiang Xu,Xiaofei Hu,Xiaoping Jin
标识
DOI:10.1016/j.biopha.2016.06.046
摘要
Atherosclerosis (AS) is associated with severe cardiovascular disease. The anti-inflammatory, anti-oxidation, and lipid regulating properties of baicalin suggest potential as an anti-atherosclerotic agent. We therefore investigated whether baicalin can protect against the development of atherosclerosis in an AS rabbit model and explored the underling mechanisms in THP-1 macrophages. In vivo, treatment with baicalin markedly decreased atherosclerotic lesion sizes and lipid accumulation in AS rabbit carotid arteries. Western blotting revealed that the protein expression levels of both peroxisome proliferator-activated receptor gamma (PPARγ) and liver X receptor alpha (LXRα) were up-regulated in the baicalin group compared with the model group. In vitro, baicalin restricted oxidized-low density lipoprotein (ox-LDL)-induced intracellular lipid accumulation and foam cell formation in THP-1 macrophages. Molecular data showed that baicalin significantly increased the expression levels of PPARγ, LXRα, ATP binding cassette transporters (ABC) A1 and ABCG1. Cell transfection experiments (including PPARγ and LXRα siRNAs) suggested that the effects of baicalin are mediated by the PPARγ-LXRα signalling pathway, which stimulates the expression of ABCA1 and ABCG1. These results suggest that baicalin potentially exerts anti-atherosclerosis effects, possibly through the PPARγ-LXRα-ABCA1/ABCG1 pathway, by promoting efflux of cholesterol from macrophages and delaying the formation of foam cells.
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