Vaccarin prevents ox-LDL-induced HUVEC EndMT, inflammation and apoptosis by suppressing ROS/p38 MAPK signaling

Oxidized low-density lipoprotein (ox-LDL)-induced endothelial-mesenchymal transition (EndMT), inflammation and apoptosis in endothelial cells play crucial roles in the progression of cardiovascular diseases including atherosclerosis. Vaccarin is a flavonoid glycoside from associated with powerful ca...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:American journal of translational research 2019-01, Vol.11 (4), p.2140-2154
Hauptverfasser: Gong, Leilei, Lei, Yueyue, Liu, Yixiao, Tan, Fanggen, Li, Shuangshuang, Wang, Xinyue, Xu, Manlin, Cai, Weiwei, Du, Bin, Xu, Fei, Zhou, Yuetao, Han, Hongxiu, Sun, Haijian, Qiu, Liying
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Oxidized low-density lipoprotein (ox-LDL)-induced endothelial-mesenchymal transition (EndMT), inflammation and apoptosis in endothelial cells play crucial roles in the progression of cardiovascular diseases including atherosclerosis. Vaccarin is a flavonoid glycoside from associated with powerful cardiovascular protective effects. However, the effects of vaccarin on human umbilical vein endothelial cells (HUVEC) injury in response to ox-LDL remain unknown. Herein, we showed that treatment with vaccarin significantly suppressed ox-LDL-induced HUVEC inflammation, EndMT and apoptosis. Mechanistically, the HUVECs exposed to ox-LDL exhibited enlarged reactive oxygen species (ROS) production and p38 MAPK phosphorylation, which was counteracted by vaccarin. Importantly, ROS activator hydrogen peroxide (H O ) and p38 MAPK activator anisomycin pretreatment prevent the protective effect of vaccarin on endothelial injury induced by ox-LDL. Our study suggested that vaccarin impeded ox-LDL-triggered HUVEC inflammation, EndMT and apoptosis via inhibition of ROS/p38 MAPK signaling pathway. Vaccarin may have a therapeutic effect on endothelial injury-related disorders.
ISSN:1943-8141
1943-8141