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

Chang Y, Chang TC, Lee JJ, Chang NC, Huang YK, Choy CS, Jayakumar T - ScientificWorldJournal (2014)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: 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.

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.

Show MeSH

Related in: MedlinePlus

Effects of SD on HG-induced phosphorylation of eNOS, ERK, and NF-κB in HUVECs: HUVECs (2 × 105 cells/well) were pretreated with SD (30 and 50 μg/mL) for 2 h and then treated with glucose (50 mM) for 30 min to detect the phosphorylation of (a) eNOS, (b) ERK1/2, and (c) NF-κB. The β-actin was used as an internal control.
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4060585&req=5

fig3: Effects of SD on HG-induced phosphorylation of eNOS, ERK, and NF-κB in HUVECs: HUVECs (2 × 105 cells/well) were pretreated with SD (30 and 50 μg/mL) for 2 h and then treated with glucose (50 mM) for 30 min to detect the phosphorylation of (a) eNOS, (b) ERK1/2, and (c) NF-κB. The β-actin was used as an internal control.

Mentions: The result showed that SD (30 and 50 μg/mL) alone had no influence on the protein expressions of phosphorylated eNOS at Ser1177, whereas high glucose leads to a significant decrease in the expression of eNOS (Figure 3(a)). Treatment with SD significantly attenuated the decreased level of eNOS expression.


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

Chang Y, Chang TC, Lee JJ, Chang NC, Huang YK, Choy CS, Jayakumar T - ScientificWorldJournal (2014)

Effects of SD on HG-induced phosphorylation of eNOS, ERK, and NF-κB in HUVECs: HUVECs (2 × 105 cells/well) were pretreated with SD (30 and 50 μg/mL) for 2 h and then treated with glucose (50 mM) for 30 min to detect the phosphorylation of (a) eNOS, (b) ERK1/2, and (c) NF-κB. The β-actin was used as an internal control.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4060585&req=5

fig3: Effects of SD on HG-induced phosphorylation of eNOS, ERK, and NF-κB in HUVECs: HUVECs (2 × 105 cells/well) were pretreated with SD (30 and 50 μg/mL) for 2 h and then treated with glucose (50 mM) for 30 min to detect the phosphorylation of (a) eNOS, (b) ERK1/2, and (c) NF-κB. The β-actin was used as an internal control.
Mentions: The result showed that SD (30 and 50 μg/mL) alone had no influence on the protein expressions of phosphorylated eNOS at Ser1177, whereas high glucose leads to a significant decrease in the expression of eNOS (Figure 3(a)). Treatment with SD significantly attenuated the decreased level of eNOS expression.

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: 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.

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.

Show MeSH
Related in: MedlinePlus