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Delphinidin‐3‐glucoside protects human umbilical vein endothelial cells against oxidized low‐density lipoprotein‐induced injury by autophagy upregulation via the AMPK/SIRT1 signaling pathway
Author(s) -
Jin Xin,
Chen Mingliang,
Yi Long,
Chang Hui,
Zhang Ting,
Wang Li,
Ma Wanqiang,
Peng Xiaoli,
Zhou Yong,
Mi Mantian
Publication year - 2014
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201400161
Subject(s) - ampk , autophagy , umbilical vein , microbiology and biotechnology , protein kinase a , chemistry , downregulation and upregulation , small interfering rna , human umbilical vein endothelial cell , endothelial stem cell , apoptosis , biology , kinase , biochemistry , transfection , gene , in vitro
Scope Oxidized LDL (oxLDL) induced vascular endothelial cell injury is a key event in the pathogenesis of atherosclerosis (AS). In our previous studies, we showed that delphinidin‐3‐glucoside (Dp), a natural anthocyanin, attenuated oxLDL‐induced injury in human umbilical vein endothelial cells (HUVECs), indicating its potential role in preventing AS. However, the involved mechanism is not fully understood. Methods and results Via methyl thiazolyl tetrazolium and flow cytometry assay, we found that Dp‐attenuated oxLDL‐induced cell viability decrease and apoptosis in HUVECs. Depending on confocal microscopy, transmission electron microscopy, and Western blot assay, we found that Dp‐induced autophagy in HUVECs, whereas suppression of autophagy significantly abolished the protective role of Dp against oxLDL‐induced endothelial cell injury. Furthermore, Dp upregulated sirtuin 1 (SIRT1) expression and SIRT1 knockdown notably suppressed Dp‐induced autophagy in HUVECs. Dp also increased the expression of phosphorylated adenosine monophosphate‐activated protein kinase, while adenosine monophosphate‐activated protein kinase (AMPK) knockdown remarkably abolished Dp‐induced SIRT1 expression and subsequent autophagy. Conclusion Our data suggested that Dp protected HUVECs against oxLDL‐induced injury by inducing autophagy via the adenosine monophosphate‐activated protein kinase/SIRT1 signaling pathway. This new finding might shed light to the prevention and therapy of AS.