Protective effect of different flavonoids against endothelial senescence via NLRP3 inflammasome

被引:12
作者
Sun, Chunhui [1 ]
Wang, Xin [1 ]
Zheng, Guihong [1 ]
Fan, Shaohua [1 ]
Lu, Jun [1 ]
Zhang, Zifeng [1 ]
Wu, Dongmei [1 ]
Shan, Qun [1 ]
Hu, Bin [1 ]
Zheng, Yuanlin [1 ]
机构
[1] Jiangsu Normal Univ, Sch Life Sci, Key Lab Biotechnol Med Plants Jiangsu Prov, Xuzhou, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
Endothelial senescence; Flavonoids; High glucose; NLRP3; inflammasome; Reactive oxygen species; CELLULAR SENESCENCE; TROXERUTIN PROTECTS; OXIDATIVE STRESS; NITRIC-OXIDE; D-GALACTOSE; REPLICATIVE SENESCENCE; MARKER PROTEIN-30; IMMUNE-RESPONSES; GENE-EXPRESSION; CELLS;
D O I
10.1016/j.jff.2016.08.031
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Senescence of vascular endothelial cells promotes endothelial dysfunction and contributes to the progression of cardiovascular diseases. It is imperative to explore effective methods to suppress endothelial senescence. Herein, we found flavonoids including quercetin, puerarin and troxerutin, which exist in normal diet and extracted from traditional herbs, delayed D-glucose-induced endothelial senescence and restored endothelial functions. In the process, D-glucose amplified endogenous reactive oxygen species (ROS) level and subsequently promoted NLRP3 inflammasome activation. However, these alterations were reversed by flavonoids. Meanwhile, clearance of ROS or interference of NLRP3 function by specific siRNA attenuated high glucose-induced senescence but advanced the anti-senescent impact of flavonoids. On the contrary, the preventive effect of flavonoids on senescence was disturbed once NLRP3 inflammasome was overactivated. Our studies suggest that flavonoids can inhibit high glucose-induced endothelial premature senescence by suppressing NLRP3 inflammasome activity, which may be a useful therapeutic strategy to alleviate endothelial senescence related vascular diseases. (C) 2016 Elsevier Ltd. All rights reserved.
引用
收藏
页码:598 / 609
页数:12
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