PMID- 27567684
OWN - NLM
STAT- MEDLINE
DCOM- 20170217
LR  - 20171116
IS  - 1879-0631 (Electronic)
IS  - 0024-3205 (Linking)
VI  - 162
DP  - 2016 Oct 1
TI  - Protection of kinsenoside against AGEs-induced endothelial dysfunction in human 
      umbilical vein endothelial cells.
PG  - 102-7
LID - S0024-3205(16)30493-3 [pii]
LID - 10.1016/j.lfs.2016.08.022 [doi]
AB  - AIMS: Kinsenoside is the major ingredient of Anoectochilus roxburghii which is a 
      traditional Chinese herb using for the treatment of diabetes. The present study 
      investigated the safety and vascular protection of kinsenoside related to 
      advanced glycation end products (AGEs) in human umbilical vein endothelial cells 
      (HUVECs) and the underlying mechanisms. MATERIALS AND METHODS: HUVECs were 
      pre-incubated with AGEs (200mug/mL) for 1h, and then co-treated with different 
      concentrations of kinsenoside (10-30mug/mL) for another 48h. After the supernatant 
      was collected, the contents of nitric oxide (NO), the levels of reactive oxygen 
      species (ROS) and inflammatory cytokines, and the expressions of AGEs receptor 
      (RAGE) and nuclear factor kappa B (NF-kappaB) were measured. KEY FINDINGS: No 
      significant changes in cell viability were found in kinsenoside-treated cells at 
      the range of 10-70mug/mL. Pretreatment with kinsenoside induced a significant 
      increase in NO production in AGEs-induced cells. In addition, kinsenoside not 
      only inhibited the expression of RAGE but also decreased intracellular ROS 
      generation induced by AGEs. Furthermore, kinsenoside suppressed the protein and 
      gene expression of NF-kappaB, and reduced the release of intercellular adhesion 
      molecule-1 (ICAM-1) and human monocyte chemoattractant protein-1 (MCP-1) in a 
      dose-dependent manner remarkably. SIGNIFICANCE: These results indicated that 
      kinsenoside might attenuate AGEs-induced endothelial dysfunction via 
      AGEs-RAGE-NF-kappaB pathway. Considering the relatively low toxicity of kinsenoside, 
      it might be a promising agent for treatment of vasculopathy in diabetic patients.
CI  - Copyright (c) 2016 Elsevier Inc. All rights reserved.
FAU - Liu, Qing
AU  - Liu Q
AD  - Department of Chemical and Pharmaceutical Engineering, College of Chemical 
      Engineering, Huaqiao University, Xiamen 361021, Fujian province, PR China. 
      Electronic address: liuq@hqu.edu.cn.
FAU - Qiao, Ai-Min
AU  - Qiao AM
AD  - Department of Chemical and Pharmaceutical Engineering, College of Chemical 
      Engineering, Huaqiao University, Xiamen 361021, Fujian province, PR China.
FAU - Yi, Li-Tao
AU  - Yi LT
AD  - Department of Chemical and Pharmaceutical Engineering, College of Chemical 
      Engineering, Huaqiao University, Xiamen 361021, Fujian province, PR China. 
      Electronic address: litaoyi@hqu.edu.cn.
FAU - Liu, Zhen-Ling
AU  - Liu ZL
AD  - State Key Laboratory of Applied Organic Chemistry, College of Chemistry and 
      Chemical Engineering, Lanzhou University, Lanzhou 730000, PR China.
FAU - Sheng, Shi-Mei
AU  - Sheng SM
AD  - Department of Chemical and Pharmaceutical Engineering, College of Chemical 
      Engineering, Huaqiao University, Xiamen 361021, Fujian province, PR China.
LA  - eng
PT  - Journal Article
DEP - 20160825
PL  - Netherlands
TA  - Life Sci
JT  - Life sciences
JID - 0375521
RN  - 0 (3-glucopyranosyloxybutanolide)
RN  - 0 (Glycation End Products, Advanced)
RN  - 0 (Monosaccharides)
RN  - OL659KIY4X (4-Butyrolactone)
SB  - IM
MH  - 4-Butyrolactone/*analogs & derivatives/pharmacology
MH  - Endothelium, Vascular/cytology/*physiopathology
MH  - *Glycation End Products, Advanced
MH  - Human Umbilical Vein Endothelial Cells
MH  - Humans
MH  - Monosaccharides/*pharmacology
MH  - Umbilical Veins/cytology/*physiopathology
OTO - NOTNLM
OT  - AGEs
OT  - Anoectochilus roxburghii
OT  - Kinsenoside
OT  - Toxicity
OT  - Vascular protection
EDAT- 2016/08/29 06:00
MHDA- 2017/02/18 06:00
CRDT- 2016/08/29 06:00
PHST- 2016/07/03 00:00 [received]
PHST- 2016/08/22 00:00 [revised]
PHST- 2016/08/23 00:00 [accepted]
PHST- 2016/08/29 06:00 [entrez]
PHST- 2016/08/29 06:00 [pubmed]
PHST- 2017/02/18 06:00 [medline]
AID - S0024-3205(16)30493-3 [pii]
AID - 10.1016/j.lfs.2016.08.022 [doi]
PST - ppublish
SO  - Life Sci. 2016 Oct 1;162:102-7. doi: 10.1016/j.lfs.2016.08.022. Epub 2016 Aug 25.