scholarly journals Effect of docosahexaenoic acid plus insulin on atherosclerotic human endothelial cells

2020 ◽  
Author(s):  
Aysan Eslami Abriz ◽  
Reza Rahbarghazi ◽  
Alireza Nourazarian ◽  
Çıgır Biray Avci ◽  
Soltan Ali Mahboob ◽  
...  

Abstract Background: Atherosclerosis is touted as one of the most critical consequences of diabetes mellitus indicated by local inflammation of endothelial cells. The Effect of Omega 3 fatty acids, mainly docosahexaenoic acid (DHA), has been investigated in cells after exposure to high doses of lipids. The current experiment aimed to address the modulatory effects of docosahexaenoic acid and insulin in palmitic-treated human endothelial cells. Methods: Human umbilical vein endothelial cells were treated with 1mM palmitic acid, 50μM insulin, 50μM docosahexaenoic acid, and their combination for 48 hours. Cell survival rate and apoptosis were measured using MTT and flow cytometry assays. The Griess assay detected NO levels. Protein levels of TNF-α, IL-6, and NF-κB were studied using ELISA and immunofluorescence imaging. The expression of genes participating in atherosclerosis was monitored using PCR array analysis. Results: Oil Red O staining showed the inhibitory effect of DHA and insulin to reduce the intracellular accumulation of palmitic acid. Both DHA and Insulin increased the reduced cell survival rate of cells after exposure to palmitic acid (p<0.05). The percent of apoptotic cells was decreased in palmitic-treated cells received insulin and DHA compared to palmitic-treated group (p<0.05). Based on our data, DHA and Insulin diminished the production of all inflammatory cytokines, TNF-α, IL-6, and NF-κB, in palmitic-treated cells (p<0.05). Similar to these data, NO production was also decreased in all groups treated with insulin and DHA compared to the palmitic-treated cells (p<0.05). PCR array analysis revealed the modulatory Effect of DHA and insulin on the expression of atherosclerosis-related genes pre-treated with palmitic acid compared to the control group (p<0.05). Conclusion: DHA and Insulin could alter the dynamic growth and dysfunctional activity of human endothelial cells after treatment with palmitic acid. Taken together, Omega 3 fatty acids, along with insulin, could dictate specific cell behavior in endothelial cells in vitro.

2020 ◽  
Author(s):  
Aysan Eslami Abriz ◽  
Reza Rahbarghazi ◽  
Alireza Nourazarian ◽  
Çıgır Biray Avci ◽  
Soltan Ali Mahboob ◽  
...  

Abstract Background: Atherosclerosis is touted as one of the most critical consequences of diabetes mellitus indicated by local inflammation of endothelial cells. The Effect of Omega 3 fatty acids, mainly docosahexaenoic acid (DHA), has been investigated in cells after exposure to high doses of lipids. The current experiment aimed to address the modulatory effects of docosahexaenoic acid and insulin in palmitic-treated human endothelial cells. Methods: Human umbilical vein endothelial cells were treated with 1mM palmitic acid, 50μM insulin, 50μM docosahexaenoic acid, and their combination for 48 hours. Cell survival rate and apoptosis were measured using MTT and flow cytometry assays. The Griess assay detected NO levels. Protein levels of TNF-α, IL-6, and NF-κB were studied using ELISA and immunofluorescence imaging. The expression of genes participating in atherosclerosis was monitored using PCR array analysis. Results: Oil Red O staining showed the inhibitory effect of DHA and insulin to reduce the intracellular accumulation of palmitic acid. Both DHA and Insulin blunted palmitic acid detrimental effects on HUVECs indicated by an increased survival rate (p<0.05). The percent of apoptotic cells was decreased in palmitic-treated cells received insulin and DHA compared to palmitic-treated group (p<0.05). Based on our data, DHA and Insulin diminished the production of all inflammatory cytokines, TNF-α, IL-6, and NF-κB, in palmitic-treated cells (p<0.05). Similar to these data, NO production was also decreased in all groups treated with insulin and DHA compared to the palmitic-treated cells (p<0.05). PCR array analysis revealed the modulatory effect of DHA and insulin on the expression of atherosclerosis-related genes pre-treated with palmitic acid compared to the control group (p<0.05). Conclusion: DHA and Insulin could alter the dynamic growth and dysfunctional activity of human endothelial cells after treatment with palmitic acid. Taken together, Omega 3 fatty acids, along with insulin, could dictate specific cell behavior in endothelial cells in vitro


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Aysan Eslami Abriz ◽  
Reza Rahbarghazi ◽  
Alireza Nourazarian ◽  
Çıgır Biray Avci ◽  
Soltan Ali Mahboob ◽  
...  

Abstract Background Atherosclerosis is touted as one of the most critical consequences of diabetes mellitus indicated by local inflammation of endothelial cells. The Effect of Omega 3 fatty acids, mainly docosahexaenoic acid (DHA), has been investigated in cells after exposure to high doses of lipids. The current experiment aimed to address the modulatory effects of docosahexaenoic acid and insulin in palmitic-treated human endothelial cells. Methods Human umbilical vein endothelial cells were treated with 1 mM palmitic acid, 50 μM insulin, 50 μM docosahexaenoic acid, and their combination for 48 h. Cell survival rate and apoptosis were measured using MTT and flow cytometry assays. The Griess assay detected NO levels. Protein levels of TNF-α, IL-6, and NF-κB were studied using ELISA and immunofluorescence imaging. The expression of genes participating in atherosclerosis was monitored using PCR array analysis. Results Oil Red O staining showed the inhibitory effect of DHA and insulin to reduce the intracellular accumulation of palmitic acid. Both DHA and Insulin blunted palmitic acid detrimental effects on HUVECs indicated by an increased survival rate (p < 0.05). The percent of apoptotic cells was decreased in palmitic-treated cells received insulin and DHA compared to palmitic-treated group (p < 0.05). Based on our data, DHA and Insulin diminished the production of all inflammatory cytokines, TNF-α, IL-6, and NF-κB, in palmitic-treated cells (p < 0.05). Similar to these data, NO production was also decreased in all groups treated with insulin and DHA compared to the palmitic-treated cells (p < 0.05). PCR array analysis revealed the modulatory effect of DHA and insulin on the expression of atherosclerosis-related genes pre-treated with palmitic acid compared to the control group (p < 0.05). Conclusion DHA and Insulin could alter the dynamic growth and dysfunctional activity of human endothelial cells after treatment with palmitic acid. Taken together, Omega 3 fatty acids, along with insulin, could dictate specific cell behavior in endothelial cells in vitro.


2018 ◽  
Vol 36 (4) ◽  
pp. 203-211 ◽  
Author(s):  
Saeede Karbasforush ◽  
Alireza Nourazarian ◽  
Masoud Darabi ◽  
Reza Rahbarghazi ◽  
Fatemeh Khaki-Khatibi ◽  
...  

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 227-227
Author(s):  
Shiqi Huang ◽  
Carla Taylor ◽  
Peter Zahradka

Abstract Objectives Angiotensin-converting enzyme 2 (ACE2) is a transmembrane protein located on the surface of endothelial cells that promotes vasodilation by promoting the hydrolysis of angiotensin II. However, ACE2 also serves as the cellular receptor for SARS-CoV-2. Infection by SARS-CoV-2 can promote endothelial dysfunction which in turn is associated with greater infection severity. Long chain omega-3 fatty acids (n3 PUFA) like eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are reported to prevent endothelial dysfunction. Thus, we hypothesize that treatment with n3 PUFA may suppress the actions of SARS-CoV-2 on endothelial cells, potentially through endothelial ACE2. The objective of the study was therefore to investigate whether changes in ACE2 levels occur as part of the endothelial response to n3 PUFA treatment. Methods Male fa/fa Zucker rats were randomised into 4 PUFA-based diet groups: α-linoleic acid (ALA), EPA, DHA, and linoleic acid (LA), for 8 weeks. EA.hy926 cells were cultured to sub-confluent and quiescent states and treated with various doses of DHA, EPA, and ALA for 8 or 24 h. ACE2 levels in tissues and cells were quantified by Western blotting. Results In contrast to ALA and EPA, DHA treatment significantly reduced ACE2 levels in rat heart, aorta, and kidney but not lungs after 8 weeks of diet intervention. EPA only showed this reduction compared to ALA in kidney. Interestingly, when applied to human endothelial cells in culture, DHA decreased ACE2 levels of growing EA.hy926 cells even at relatively low doses, but no significant effect was observed in quiescent cells. EPA also had an effect, but only at an extremely high dose. Conclusions DHA reduced ACE2 levels in key organs and human endothelial cells, which should produce beneficial effects by lowering the susceptibility of cells to SARS-CoV-2. Funding Sources St Boniface Hospital Foundation - Research Without Borders and University of Manitoba - GETS


2018 ◽  
Vol 119 (12) ◽  
pp. 9752-9763 ◽  
Author(s):  
Tannaz Novinbahador ◽  
Alireza Nourazarian ◽  
Mohammad Asgharzadeh ◽  
Reza Rahbarghazi ◽  
Çıgır Biray Avci ◽  
...  

2005 ◽  
Vol 73 (6) ◽  
pp. 3271-3277 ◽  
Author(s):  
Nicola K. Viebig ◽  
Ulrich Wulbrand ◽  
Reinhold Förster ◽  
Katherine T. Andrews ◽  
Michael Lanzer ◽  
...  

ABSTRACT Cytoadherence of Plasmodium falciparum-infected erythrocytes (PRBC) to endothelial cells causes severe clinical disease, presumably as a of result perfusion failure and tissue hypoxia. Cytoadherence to endothelial cells is increased by endothelial cell activation, which is believed to occur in a paracrine fashion by mediators such as tumor necrosis factor alpha (TNF-α) released from macrophages that initially recognize PRBC. Here we provide evidence that PRBC directly stimulate human endothelial cells in the absence of macrophages, leading to increased expression of adhesion-promoting molecules, such as intercellular adhesion molecule 1. Endothelial cell stimulation by PRBC required direct physical contact for a short time (30 to 60 min) and was correlated with parasitemia. Gene expression profiling of endothelial cells stimulated by PRBC revealed increased expression levels of chemokine and adhesion molecule genes. PRBC-stimulated endothelial cells especially showed increased expression of molecules involved in parasite adhesion but failed to express molecules promoting leukocyte adhesion, such as E-selectin and vascular cell adhesion molecule 1, even after challenge with TNF-α. Collectively, our data suggest that stimulation of endothelial cells by PRBC may have two effects: prevention of parasite clearance through increased cytoadherence and attenuation of leukocyte binding to endothelial cells, thereby preventing deleterious immune reactivity.


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