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. Issue 10 (22nd July 2014)
- Record Type:
- Journal Article
- Title:
- 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. Issue 10 (22nd July 2014)
- Main Title:
- 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
- Authors:
- Jin, Xin
Chen, Mingliang
Yi, Long
Chang, Hui
Zhang, Ting
Wang, Li
Ma, Wanqiang
Peng, Xiaoli
Zhou, Yong
Mi, Mantian - Abstract:
- <abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="mnfr2229-sec-0010" sec-type="section"> <title>Scope</title> <p>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.</p> </sec> <sec id="mnfr2229-sec-0020" sec-type="section"> <title>Methods and results</title> <p>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.</p> </sec> <sec id="mnfr2229-sec-0030"<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="mnfr2229-sec-0010" sec-type="section"> <title>Scope</title> <p>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.</p> </sec> <sec id="mnfr2229-sec-0020" sec-type="section"> <title>Methods and results</title> <p>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.</p> </sec> <sec id="mnfr2229-sec-0030" sec-type="section"> <title>Conclusion</title> <p>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.</p> </sec> </abstract> … (more)
- Is Part Of:
- Molecular nutrition & food research. Volume 58:Issue 10(2014:Oct.)
- Journal:
- Molecular nutrition & food research
- Issue:
- Volume 58:Issue 10(2014:Oct.)
- Issue Display:
- Volume 58, Issue 10 (2014)
- Year:
- 2014
- Volume:
- 58
- Issue:
- 10
- Issue Sort Value:
- 2014-0058-0010-0000
- Page Start:
- 1941
- Page End:
- 1951
- Publication Date:
- 2014-07-22
- Subjects:
- Food -- Biotechnology -- Periodicals
Food -- Microbiology -- Periodicals
Nutrition -- Periodicals
Food -- Toxicology -- Periodicals
Nutrition -- Periodicals
Food Microbiology -- Periodicals
Food Technology -- Periodicals
Molecular Biology -- Periodicals
664.0705 - Journal URLs:
- http://onlinelibrary.wiley.com/ ↗
- DOI:
- 10.1002/mnfr.201400161 ↗
- Languages:
- English
- ISSNs:
- 1613-4125
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 5900.817992
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 3461.xml