PMID- 30372883
OWN - NLM
STAT- MEDLINE
DCOM- 20190318
LR  - 20190318
IS  - 1950-6007 (Electronic)
IS  - 0753-3322 (Linking)
VI  - 108
DP  - 2018 Dec
TI  - Vildagliptin protects endothelial cells against high glucose-induced damage.
PG  - 1790-1796
LID - S0753-3322(18)34228-8 [pii]
LID - 10.1016/j.biopha.2018.09.148 [doi]
AB  - Hyperglycemia or high blood sugar is one of the major pathological 
      characteristics of diabetes. The endothelium is the inner layer of the vascular 
      wall and is directly exposed to various stimuli in blood vessels. As a 
      characteristic of diabetes, chronic high glucose is known to be harmful to 
      endothelial cells. In this study, we found that vildagliptin, an available type 2 
      diabetes agent, protects primary human aortic endothelial cells (HAECs) against 
      damage induced by high glucose. Our data indicate that vildagliptin improves the 
      decrease in endothelial viability and reduces the release of lactate 
      dehydrogenase (LDH) induced by high glucose. Vildagliptin potently suppresses 
      high glucose-induced generation of reactive oxygen species (ROS) and production 
      of vascular inflammatory factors including tumor necrosis factor-alpha (TNF-alpha), 
      interleukin-8 (IL-8), intercellular cell adhesion molecule-1 (ICAM-1) and 
      monocyte chemotactic protein 1 (MCP-1). Moreover, vildagliptin suppresses 
      adhesion of monocytes to endothelial cells and induction of toll-like receptor 4 
      (TLR-4) in HAECs caused by high glucose. Mechanistically, we found that the 
      cellular protective effects mediated by vildagliptin involve suppression of 
      nuclear factor-kappa B (NF-kappaB) nuclear signals. Collectively, our data indicate 
      that vildagliptin possesses a protective function in vascular cells.
CI  - Copyright (c) 2018. Published by Elsevier Masson SAS.
FAU - Zhang, Meng
AU  - Zhang M
AD  - Department of Cardiology, Affiliated Hospital of Jining Medical University, 
      Jining, 272000, China.
FAU - Jin, Xin
AU  - Jin X
AD  - Department of Cardiology, Affiliated Hospital of Jining Medical University, 
      Jining, 272000, China.
FAU - Zhang, Zonglei
AU  - Zhang Z
AD  - Department of Cardiology, Affiliated Hospital of Jining Medical University, 
      Jining, 272000, China.
FAU - Li, Bin
AU  - Li B
AD  - Department of Cardiology, Affiliated Hospital of Jining Medical University, 
      Jining, 272000, China.
FAU - Yang, Guoliang
AU  - Yang G
AD  - Department of Cardiology, Affiliated Hospital of Jining Medical University, 
      Jining, 272000, China. Electronic address: yao025zh@21cn.com.
LA  - eng
PT  - Journal Article
DEP - 20181016
PL  - France
TA  - Biomed Pharmacother
JT  - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
JID - 8213295
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (NF-kappa B)
RN  - 0 (Protective Agents)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (TLR4 protein, human)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - I6B4B2U96P (Vildagliptin)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Cell Adhesion/drug effects
MH  - Cell Line
MH  - Cell Survival/drug effects
MH  - Chemokine CCL2/genetics/metabolism
MH  - Cytokines/metabolism
MH  - Cytoprotection/*drug effects
MH  - Endothelial Cells/drug effects/metabolism/*pathology
MH  - Glucose/*toxicity
MH  - Humans
MH  - Membrane Potential, Mitochondrial/drug effects
MH  - NF-kappa B/metabolism
MH  - Protective Agents/pharmacology
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction/drug effects
MH  - Toll-Like Receptor 4/metabolism
MH  - Vascular Cell Adhesion Molecule-1/genetics/metabolism
MH  - Vildagliptin/chemistry/*pharmacology
OTO - NOTNLM
OT  - Endothelial damage
OT  - High glucose
OT  - NF-kappaB pathway
OT  - Toll-like receptor 4 (TLR-4)
OT  - Vildagliptin
EDAT- 2018/10/31 06:00
MHDA- 2019/03/19 06:00
CRDT- 2018/10/31 06:00
PHST- 2018/06/26 00:00 [received]
PHST- 2018/09/14 00:00 [revised]
PHST- 2018/09/26 00:00 [accepted]
PHST- 2018/10/31 06:00 [pubmed]
PHST- 2019/03/19 06:00 [medline]
PHST- 2018/10/31 06:00 [entrez]
AID - S0753-3322(18)34228-8 [pii]
AID - 10.1016/j.biopha.2018.09.148 [doi]
PST - ppublish
SO  - Biomed Pharmacother. 2018 Dec;108:1790-1796. doi: 10.1016/j.biopha.2018.09.148. 
      Epub 2018 Oct 16.