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ScientificWorldJournal. 2014;2014:423259. doi: 10.1155/2014/423259. Epub 2014 Jun 2.

Sanguis draconis, a dragon's blood resin, attenuates high glucose-induced oxidative stress and endothelial dysfunction in human umbilical vein endothelial cells.

Author information

1
Department of Anesthesiology, Shin Kong Wu Ho-Su Memorial Hospital, 95 Wen-Chang Road, Taipei 101, Taiwan ; School of Medicine, Fu-Jen Catholic University, 510 Zhong-Zheng Road, Taipei 205, Taiwan ; Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.
2
Department of Lymphatic Vascular Surgery, Wan Fang Hospital, Taipei Medical University, Taipei 110, Taiwan.
3
Department of Pharmacology, Taipei Medical University, Taipei 110, Taiwan ; Department of Surgery, Mackay Memorial Hospital, Taipei 104, Taiwan ; Mackay Junior College of Medicine, Nursing, and Management, Taipei 112, Taiwan.
4
Department of Cardiology, School of Medicine, Taipei Medical University, Taipei 110, Taiwan.
5
School of Oral Hygiene, College of Oral Medicine, Taipei Medical University, Taipei 110, Taiwan.
6
Emergency and Intensive Care Department, Min-Sheng Hospital 168, Taoyuan 330, Taiwan ; Department of Medicine, Taipei Medical University, Taipei 110, Taiwan.
7
Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 110, Taiwan ; Department of Pharmacology, Taipei Medical University, Taipei 110, Taiwan.

Abstract

Hyperglycaemia, a characteristic feature of diabetes mellitus, induces endothelial dysfunction and vascular complications by limiting the proliferative potential of these cells. Here we aimed to investigate the effect of an ethanolic extract of Sanguis draconis (SD), a kind of dragon's blood resin that is obtained from Daemonorops draco (Palmae), on human umbilical vein endothelial cells (HUVEC) under high-glucose (HG) stimulation and its underlying mechanism. Concentration-dependent (0-50 μg/mL) assessment of cell viability showed that SD does not affect cell viability with a similar trend up to 48 h. Remarkably, SD (10-50 μg/mL) significantly attenuated the high-glucose (25 and 50 mM) induced cell toxicity in a concentration-dependent manner. SD inhibited high glucose-induced nitrite (NO) and lipid peroxidation (MDA) production and reactive oxygen species (ROS) formation in HUVEC. Western blot analysis revealed that SD treatments abolished HG-induced phosphorylation of extracellular signal-regulated kinase 1/2 (ERK 1/2), nuclear transcription factor, κB (NF-κB), VCAM-1, and E-selectin, and it also blocked the breakdown of PARP-116 kDa protein in a dose-dependent manner. Furthermore, we found that SD increased the expression of Bcl-2 and decreased Bax protein expression in HG-stimulated HUVEC. Thus, these results of this study demonstrate for the first time that SD inhibits glucose induced oxidative stress and vascular inflammation in HUVEC by inhibiting the ERK/NF-κB/PARP-1/Bax signaling cascade followed by suppressing the activation of VCAM-1 and E-selectin. These data suggest that SD may have a therapeutic potential in vascular inflammation due to the decreased levels of oxidative stress, apoptosis, and PARP-1 activation.

PMID:
24987732
PMCID:
PMC4060585
DOI:
10.1155/2014/423259
[Indexed for MEDLINE]
Free PMC Article

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