333 ANGIOTENSIN II-INDUCED RAPID PHASE INCREASE IN VASCULAR ENDOTHELIAL GROWTH FACTOR SYNTHESIS IN RENAL TUBULAR EPITHELIAL CELLS IS DEPENDENT ON REACTIVE OXYGEN SPECIES PRODUCTION

2005 ◽  
Vol 53 (1) ◽  
pp. S312.4-S312
Author(s):  
D. Feliers ◽  
Y. Gorin ◽  
Ghosh G. Choudhury ◽  
H. E. Abboud ◽  
B. S. Kasinath
2018 ◽  
Vol 16 (1) ◽  
pp. 298-305
Author(s):  
Ming Wu ◽  
Min Hu ◽  
Huansheng Tong ◽  
Junying Liu ◽  
Hui Jiang ◽  
...  

AbstractKidney ischemia and hypoxia can cause renal cell apoptosis and activation of inflammatory cells, which lead to the release of inflammatory factors and ultimately result in the damage of kidney tissue and the whole body. Renal tubular cell and macrophage autophagy can reduce the production of reactive oxygen species (ROS), thereby reducing the activation of inflammatory cytoplasm and its key effector protein, caspase-1, which reduces the expression of IL-1β and IL-18 and other inflammatory factors. Ulinastatin (UTI), as a glycoprotein drug, inhibits the activity of multiple proteases and reduces myocardial damage caused by ischemia-reperfusion by upregulating autophagy. However, it can be raised by macrophage autophagy, reduce the production of ROS, and ultimately reduce the expression of inflammatory mediators, thereby reducing renal cell injury, promote renal function recovery is not clear. In this study, a series of cell experiments have shown that ulinastatin is reduced by regulating the autophagy of renal tubular epithelial cells and macrophages to reduce the production of reactive oxygen species and inflammatory factors (TNF-α, IL-1β and IL-1), and then, increase the activity of the cells under the sugar oxygen deprivation model. The simultaneous use of cellular autophagy agonists Rapamycin (RAPA) and ulinastatin has a synergistic effect on the production of reactive oxygen species and the expression of inflammatory factors.


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.


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