scholarly journals Signaling pathway of ginsenoside-Rg1 leading to nitric oxide production in endothelial cells

FEBS Letters ◽  
2006 ◽  
Vol 580 (13) ◽  
pp. 3211-3216 ◽  
Author(s):  
Kar Wah Leung ◽  
Yuen-Kit Cheng ◽  
Nai Ki Mak ◽  
Kelvin K.C. Chan ◽  
T.P. David Fan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Signaling Pathway ◽  
Nitric Oxide Production ◽  
Ginsenoside Rg1 ◽  
Oxide Production

Resveratrol and grape juice: Effects on redox status and nitric oxide production of endothelial cells in in vitro preeclampsia model

2021 ◽  
Vol 23 ◽  
pp. 205-210
Author(s):  
Mayara Caldeira-Dias ◽  
Sarah Viana-Mattioli ◽  
Jackeline de Souza Rangel Machado ◽  
Mattias Carlström ◽  
Ricardo de Carvalho Cavalli ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Grape Juice ◽  
Redox Status ◽  
Nitric Oxide Production ◽  
Oxide Production

scholarly journals Effects of Propofol on Cyclic Strain-induced Endothelin-1 Expression in Human Umbilical Vein Endothelial Cells

2009 ◽  
Vol 110 (1) ◽  
pp. 74-80 ◽  
Author(s):  
Tzu-Hurng Cheng ◽  
Jin-Jer Chen ◽  
Cheng-Hsien Chen ◽  
Kar-Lok Wong
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Protein Kinase ◽  
Umbilical Vein ◽  
Cyclic Strain ◽  
Nitric Oxide Production ◽  
Human Umbilical Vein ◽  
Oxide Production ◽  
Extracellular Signal ◽  
Umbilical Vein Endothelial Cells

Background Propofol is one of the most popular intravenous induction agents of general anesthesia. Experimental results revealed that propofol exerted hypotensive and antioxidative effects. However, the intracellular mechanism of propofol remains to be delineated. The aims of this study were to test the hypothesis that propofol may alter strain-induced endothelin-1 (ET-1) secretion and nitric oxide production, and to identify the putative underlying signaling pathways in human umbilical vein endothelial cells. Methods Cultured human umbilical vein endothelial cells were exposed to cyclic strain in the presence of propofol, and ET-1 expression was examined by Northern blotting and enzyme-linked immunosorbent assay kit. Activation of extracellular signal-regulated protein kinase, endothelial nitric oxide synthase, and protein kinase B were assessed by Western blot analysis. Results The authors show that propofol inhibits strain-induced ET-1 expression, strain-increased reactive oxygen species formation, and extracellular signal-regulated protein kinase phosphorylation. On the contrary, nitric oxide production, endothelial nitric oxide synthase activity, and protein kinase B phosphorylation were enhanced by propofol treatment. Furthermore, in the presence of PTIO, a nitric oxide scavenger, and KT5823, a specific inhibitor of cyclic guanosine monophosphate-dependent protein kinase, the inhibitory effect of propofol on strain-induced extracellular signal-regulated protein kinase phosphorylation and ET-1 release was reversed. Conclusions The authors demonstrate for the first time that propofol inhibits strain-induced ET-1 secretion and enhances strain-increased nitric oxide production in human umbilical vein endothelial cells. Thus, this study delivers important new insight into the molecular pathways that may contribute to the proposed hypotensive effects of propofol in the cardiovascular system.

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