脂肪变性
脂肪变
巨噬细胞
胆固醇逆向转运
硫氧还蛋白
化学
胆固醇
细胞生物学
生物化学
生物
脂肪肝
内科学
内分泌学
医学
脂蛋白
氧化应激
体外
疾病
作者
Xiong Wang,Haikang Zhao,Wenjun Yan,Yi Liu,Tao Yin,Shan Wang,Min Fan,Congye Li,Ling Zhang,Ling Tao
标识
DOI:10.1016/j.bbrc.2019.06.109
摘要
Atherosclerosis is characterized by the accumulation of excess cholesterol in plaques. Reverse cholesterol transport (RCT) plays a key role in the removal of cholesterol. In the present study, we examined the effect of thioredoxin-1 (Trx-1) on RCT and explored the underlying mechanism. We found that Trx-1 promoted RCT in vivo, as did T0901317, a known liver X receptor (LXR) ligand. T0901317 also inhibited the development of atherosclerotic plaques but promoted liver steatosis. Furthermore, Trx-1 promoted macrophage cholesterol efflux to apoAI in vitro. Mechanistically, Trx-1 promoted nuclear translocation of LXRα and induced the expression of ATP-binding cassette transporter A1 (ABCA1). Apolipoprotein E knockout (apoE−/−) mice fed an atherogenic diet were daily injected intraperitoneally with saline or Trx-1 (0.33 mg/kg). Trx-1 treatment significantly inhibited the development of atherosclerosis and induced the expression of ABCA1 in macrophages retrieved from apoE−/− mice. Moreover, the liver steatosis was attenuated by Trx-1. Overall, we demonstrated that Trx-1 promotes RCT by upregulating ABCA1 expression through induction of nuclear translocation of LXRα, and protects liver from steatosis.
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