scholarly journals Sanguinarine Inhibits Vascular Endothelial Growth Factor Release by Generation of Reactive Oxygen Species in MCF-7 Human Mammary Adenocarcinoma Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Xian-zhe Dong ◽  
Miao Zhang ◽  
Kun Wang ◽  
Ping Liu ◽  
Dai-hong Guo ◽  
...  

The inhibitory action and the possible mechanism of anticancer compound Sanguinarine (SAN) on vascular endothelial growth factor (VEGF) in human mammary adenocarcinoma cells MCF-7 were evaluated in this study. We exposed MCF-7 to SAN for 24 h, then cell viability was assessed by using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction assay. Human VEGF was measured using a paired antibody quantitative ELISA kit, relative expression of VEGF mRNA was calculated using the real-time PCR studies, and the effect of SAN on the reactive oxygen species (ROS) level was detected by the flow cytometer. Treatment with SAN remarkably inhibited growth of MCF-7 cells and induced cell apoptosis. We found that VEGF release was stimulated by subtoxic concentrations of SAN and inhibited by high dose of SAN, SAN-evoked VEGF release was mimicked by low concentration of H2O2, and SAN-regulated VEGF inhibition was accompanied by increasing of ROS; these changes were abolished by antioxidant. High concentration of SAN inhibited VEGF mRNA expression in MCF-7 cultures, suggesting an effect at transcriptional level, and was also abolished by antioxidant. The present findings indicated that the regulation of VEGF expression and release from MCF-7 cells were possibly through reactive oxygen species evoked by SAN.

2017 ◽  
Vol 35 (1) ◽  
pp. 65
Author(s):  
Kanjana Jittiporn ◽  
Wisuda Suvitayavat ◽  
Primchanien Moongkarndi ◽  
Rulth B Caldwell

Objective: This study aimed to determine the effect of mangosteen extract on hypoxia induced reactive oxygen species production and vascular endothelial growth factor (VEGF) induced retinal endothelial cell migration.Material and Method: This research studied bovine retinal endothelial cells. The non-toxic concentration of mangosteen extract of water soluble part was verified using trypan blue staining. The effects of mangosteen extract on hypoxia induced reactive oxygen species production and retinal endothelial cells migration were determined using 2’, 7’ dichlorodihydrofluorescein diacetate and scrape/wound assay, respectively. The mechanism of mangosteen extract on retinal endothelial cell migration was determined using western blotting. The analysis of variance was used to determine the differences among group means.Results: The concentrations of mangosteen extract at 25, 50 and 100 mg/ml were non-toxic and these concentrations were used in further experiments. Mangosteen extract at a dose of 100 mg/ml significantly attenuated hypoxia induced reactive oxygen species formation. At all doses, mangosteen extract also significantly inhibited retinal endothelial cell migration. However, the mechanism of mangosteen extract on VEGF signaling did not affect the phosphorylation of VEGF receptor 2 (VEGFR2).Conclusion: Mangosteen extract has anti-oxidant and anti-migration effects.


2007 ◽  
Vol 67 (22) ◽  
pp. 10823-10830 ◽  
Author(s):  
Chang Xia ◽  
Qiao Meng ◽  
Ling-Zhi Liu ◽  
Yongyut Rojanasakul ◽  
Xin-Ru Wang ◽  
...  

2001 ◽  
Vol 280 (4) ◽  
pp. L585-L592 ◽  
Author(s):  
Ioanna Kosmidou ◽  
Angeliki Xagorari ◽  
Charis Roussos ◽  
Andreas Papapetropoulos

Vascular endothelial growth factor (VEGF) is a potent angiogenic stimulus, the expression of which increases in skeletal muscle after exercise. Because exercise is also accompanied by increased intramuscular reactive oxygen species (ROS) generation, we tested the hypothesis that ROS stimulate VEGF production from skeletal myotubes. Differentiated C2C12skeletal myotubes exposed to ROS-producing agents exhibited a concentration-dependent increase in VEGF production, whereas undifferentiated myoblasts did not respond to oxidants. Moreover, conditioned medium from ROS-treated myotubes increased the bovine lung microvascular cell proliferation rate. To study the mechanism(s) involved in the stimulation of VEGF production by ROS, myotubes were pretreated with a selective phosphatidylinositol 3-kinase (PI3K) inhibitor, LY-294002, before being exposed to hydrogen peroxide or pyrogallol. LY-294002 attenuated both Akt phosphorylation and VEGF production. In addition, oxidants increased nuclear factor-κB-dependent promoter activity in transiently transfected myotubes; however, pretreatment with the pharmacological inhibitor of nuclear factor-κB, diethyldithiocarbamate, did not affect the oxidant-stimulated VEGF release. We conclude that ROS induce VEGF release from myotubes via a PI3K/Akt-dependent pathway.


Sign in / Sign up

Export Citation Format

Share Document