Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 532, Issue 3, Pages 466-474Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2020.08.076
Keywords
Celastrol; Vascular smooth muscle cells; Lipid accumulation; LXR alpha/ABCA1 signaling pathway; Autophagy; Atherosclerosis
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Funding
- National Natural Science Foundation of China [81973668, 81774130, 81670268, 81603600]
- Natural Science Foundation for Distinguished Young Scholars of Hunan Province [2018JJ1018]
- Pharmaceutical Open Fund of Domestic First-class Disciplines (cultivation) of Hunan Province [2018YX01]
- Natural Science Foundation of Guangdong Province [2016A030313026]
- Hunan Provincial Key Discipline of Pharmaceutical Science
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The uptake of modified low-density lipoprotein (LDL) and the accumulation of lipid droplets induce the formation of vascular smooth muscle cells (VSMCs)-derived foam cells, thereby promoting the development and maturation of plaques and accelerating the progression of atherosclerosis. Celastrol is a quinine methide triterpenoid isolated from the root bark of traditional Chinese herb Tripterygium wilfordii. It possesses various biological properties, including anti-obesity, cardiovascular protection, anti-inflammation, etc. In the present study, we found that celastrol significantly reduced lipid accumulation induced by oxidized LDL (ox-LDL) in VSMCs. Mechanistically, celastrol up-regulated adenosine triphosphate-binding cassette transporter A1 (ABCA1 ) expression through activating liver X receptor alpha (LXR alpha) expression, which contributed to inhibit lipid accumulation in VSMCs. Meanwhile, celastrol decreased lipid accumulation by triggering autophagy in VSMCs. Therefore, these findings supported celastrol as a potentially effective agent for the prevention and therapy of atherosclerosis. (C) 2020 Elsevier Inc. All rights reserved.
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