Effects of AFP-172 on COX-2-induced angiogenic activities on human umbilical vein endothelial cells

2012 ◽  
Vol 250 (12) ◽  
pp. 1765-1775 ◽  
Author(s):  
Young Jung Roh ◽  
Young Gun Park ◽  
Seungbum Kang ◽  
Soo Young Kim ◽  
Jung Il Moon
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Cox 2 ◽  
Umbilical Vein Endothelial Cells

scholarly journals Evaluation of Anti-Inflammatory Components of Guizhi Fuling Capsule, an Ancient Chinese Herbal Formula, in Human Umbilical Vein Endothelial Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
Yuzhong Zheng ◽  
Guizhong Xin ◽  
Guowei Gong ◽  
Tina TX Dong ◽  
Ping Li ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Active Components ◽  
Human Umbilical Vein ◽  
Cellular Inflammation ◽  
Cyclooxygenase 1 ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Umbilical Vein Endothelial Cells ◽  
Cox 1

Background. Guizhi Fuling capsule (GFC), a well-known formula composed of five medicinal herbs, is commonly prescribed to treat primary dysmenorrhea, as well as to achieve good clinical efficacy in China. However, the active components of GFC have not been identified. Here, the anti-inflammatory functions of GFC, as well as its major ingredients, were evaluated in human umbilical vein endothelial cells (HUVECs). Methods. Lipopolysaccharide (LPS) was used in HUVECs to imitate the cellular inflammation. Then, GFC-triggered mRNA expressions of cyclooxygenase-1 (COX-1) and COX-2 were determined by real-time PCR, while the expression of COX-2 protein was revealed by western blotting. Besides, nine components of GFC were evaluated for their contribution value in the anti-dysmenorrhea effects Results. The application of GFC downregulated the mRNA expressions of COX-1 and COX-2 mRNAs. Nine major components of GFC were tested in the inflammatory system, and three compounds, including paeoniflorin, benzoylpaeoniflorin, and amygdalin, exhibited robust activation in HUVECs. The combination of paeoniflorin, benzoylpaeoniflorin, and amygdalin showed over 80% of the anti-inflammatory activation. Conclusion. Our study supports that GFC plays a promising role in anti-dysmenorrhea function by decreasing COXs’ expression. Besides, paeoniflorin, benzoylpaeoniflorin, and amygdalin could be considered as major regulators for the anti-dysmenorrhea effects of GFC.

Regulation of PGE2and PGI2release from human umbilical vein endothelial cells by actin cytoskeleton

2001 ◽  
Vol 281 (3) ◽  
pp. C1038-C1045 ◽  
Author(s):  
Sara J. Sawyer ◽  
Suzanne M. Norvell ◽  
Suzanne M. Ponik ◽  
Fredrick M. Pavalko
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Specific Inhibitor ◽  
Fold Increase ◽  
Prostaglandin E ◽  
Microtubule Network ◽  
Human Umbilical Vein ◽  
Drug Treatments ◽  
Cox 2 ◽  
Umbilical Vein Endothelial Cells

Disruption of microfilaments in human umbilical vein endothelial cells (HUVEC) with cytochalasin D (cytD) or latrunculin A (latA) resulted in a 3.3- to 5.7-fold increase in total synthesis of prostaglandin E2(PGE2) and a 3.4- to 6.5-fold increase in prostacyclin (PGI2) compared with control cells. Disruption of the microtubule network with nocodazole or colchicine increased synthesis of PGE21.7- to 1.9-fold and PGI21.9- to 2.0-fold compared with control cells. Interestingly, however, increased release of PGE2and PGI2from HUVEC into the media occurred only when microfilaments were disrupted. CytD treatment resulted in 6.7-fold more PGE2and 3.8-fold more PGI2released from HUVEC compared with control cells; latA treatment resulted in 17.7-fold more PGE2and 11.2-fold more PGI2released compared with control cells. Both increased synthesis and release of prostaglandins in response to all drug treatments were completely inhibited by NS-398, a specific inhibitor of cyclooxygenase-2 (COX-2). Disruption of either microfilaments using cytD or latA or of microtubules using nocodazole or colchicine resulted in a significant increase in COX-2 protein levels, suggesting that the increased synthesis of prostaglandins in response to drug treatments may result from increased activity of COX-2. These results, together with studies demonstrating a vasoprotective role for prostaglandins, suggest that the cytoskeleton plays an important role in maintenance of endothelial barrier function by regulating prostaglandin synthesis and release from HUVEC.

scholarly journals Effects of Insulin-Like Growth Factor I and II on Prostaglandin Synthesis and Plasminogen Activator Activity in Human Umbilical Vein Endothelial Cells

2005 ◽  
Vol 90 (1) ◽  
pp. 372-378 ◽  
Author(s):  
Fiorella Miceli ◽  
Anna Tropea ◽  
Francesca Minici ◽  
Mariateresa Orlando ◽  
Giuseppina Lamanna ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Colorimetric Assay ◽  
Umbilical Vein ◽  
Vascular Diseases ◽  
Potential Effect ◽  
Human Umbilical Vein ◽  
Cox 2 ◽  
Umbilical Vein Endothelial Cells ◽  
Pai 1

Abstract IGFs seem to contribute to the endothelial dysfunction observed in some vascular diseases. Because locally increased IGFs levels were detected in the preeclamptic fetoplacental unit, we hypothesized their involvement in the dysregulation of fibrinolysis and vascular tone typically observed in the fetoplacental compartment in this pregnancy disease. Therefore, in human umbilical vein endothelial cells (HUVECs), the potential effect of IGFs on the synthesis of plasminogen activators (PAs), PA inibitor-1 (PAI-1), and vasodilator and vasoconstrictor prostaglandins (PGs) was investigated. Moreover, in HUVECs treated with IGFs, the expression of cyclooxygenase (COX)-2, the rate-limiting enzyme in PG synthesis, was evaluated. HUVECs were treated for 24 h with IGFs (1–100 ng/ml) or IL-1β (0.1 ng/ml). PA, PAI-1, and COX-2 mRNA was determined by RT-PCR and PG release and PA activity by RIA and colorimetric assay, respectively. We demonstrated an inhibition of urokinase-type PA activity and a 50% reduction of urokinase-type PA mRNA in HUVECs treated with IGFs. No effect was seen on PAI-1. Finally, both IGFs significantly decreased all PGs tested and COX-2 mRNA, whereas, as expected, IL-1β had an opposite effect. In conclusion, our results suggest for IGFs a potential involvement in the endothelial dysfunction observed in preeclamptic fetoplacental unit.

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