scholarly journals Effect of anthocyanin-rich sour cherry extract on the level of IL-8 in LPS-induced endothelial cell

2020 ◽  
pp. 27-30
Author(s):  
Attila Biró ◽  
Arnold Markovics ◽  
László Stündl ◽  
Judit Remenyik
Keyword(s):  
Endothelial Cells ◽  
Inflammatory Diseases ◽  
Sour Cherry ◽  
Tetrazolium Salt ◽  
Human Umbilical Cord ◽  
Anthocyanin Content ◽  
Umbilical Cord Vein ◽  
Lps Treatment ◽  
Human Umbilical Cord Vein ◽  
Inflammatory Effect

The anthocyanin content of the Hungarian sour cherry is remarkable. Nutraceutical and pharmaceutical effects of the anthocyanins and their role in disease prevention have been studied extensively. Endothelial cells are involved in the pathogenesis of several inflammatory diseases. The objective of this work was to investigate pure sour cherry extract on human umbilical cord vein endothelial cells (HUVECs) as an inflammatory model.  HUVECs were treated with 100 ng/mL lipopolysaccharide (LPS) and 50 mg/mL sour cherry extract or M199 medium as control. The optimal concentration range of the sour cherry extract was investigated and selected based on MTT assay measuring the conversion of the tetrazolium salt to formazan by mitochondrial dehydrogenases. The level of interleukine-8 (IL-8), a pro-inflammatory cytokine, was measured in Luminex MagPlex assay. LPS treatment significantly increased the secretion of IL-8. The pure sour cherry extract was able to attenuate this increment indicating the potent anti-inflammatory effect of pure sour cherry extract. Our results emphasize that pure sour cherry extract could reduce the LPS-induced inflammatory response thereby may improve endothelial dysfunction.

Oncostatin M regulates endothelin-1 production in human endothelial cells

1998 ◽  
Vol 275 (2) ◽  
pp. H662-H667 ◽  
Author(s):  
Outi Saijonmaa ◽  
Tuulikki Nyman ◽  
Päivi Pacek ◽  
Frej Fyhrquist
Keyword(s):  
Endothelial Cells ◽  
Tyrosine Kinase ◽  
Kinase Inhibitors ◽  
Oncostatin M ◽  
Human Umbilical Cord ◽  
Kinase Activation ◽  
Endothelin 1 ◽  
Umbilical Cord Vein ◽  
Pkc Activation ◽  
Human Umbilical Cord Vein

The effect of the macrophage- and T-lymphocyte-derived cytokine oncostatin M (OSM) on endothelin-1 (ET-1) production in cultured human umbilical cord vein endothelial cells (HUVEC) was studied. OSM (2.5–10 ng/ml) stimulated ET-1 production and the expression of preproendothelin-1 mRNA. The stimulatory effect of OSM was reversed by anti-interleukin (IL)-6 IgG (33 μg/ml). IL-6 (10 ng/ml) was shown to stimulate ET-1 production. The tyrosine kinase inhibitors herbimycin (250–500 ng/ml) and genistein (1–4 μg/ml) suppressed basal ET-1 production and reversed the stimulatory effect of OSM, whereas daidzein (1–8 μg/ml), a less active analog of genistein, had no effect on basal ET-1 production and only partly reversed the stimulatory effect of OSM. The phorbol ester phorbol 12-myristate 13-acetate (PMA) inhibited ET-1 production. Downregulation of protein kinase C (PKC) with PMA (1 μM) preincubation potentiated OSM-induced ET-1 production. In summary, OSM stimulated ET-1 production in cultured HUVEC. The stimulation was probably mediated by IL-6. Furthermore, the present data suggest that tyrosine kinase activation was involved in ET-1 stimulation and that PKC activation leads to suppression of basal and OSM-stimulated ET-1 production.

Atorvastatin completely inhibits VEGF-induced ACE upregulation in human endothelial cells

2004 ◽  
Vol 286 (6) ◽  
pp. H2096-H2102 ◽  
Author(s):  
Outi Saijonmaa ◽  
Tuulikki Nyman ◽  
Pia Stewen ◽  
Frej Fyhrquist
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Cells ◽  
Kinase Inhibitor ◽  
Mevalonate Pathway ◽  
Suppressive Effect ◽  
Human Umbilical Cord ◽  
Human Endothelial Cells ◽  
Prevention And Treatment ◽  
Umbilical Cord Vein ◽  
Human Umbilical Cord Vein

Angiotensin-converting enzyme (ACE) plays an important role in the pathophysiology of cardiovascular disease. We investigated whether atorvastatin, a powerful agent for the prevention and treatment of cardiovascular disease, influences ACE production in endothelial cells. Human umbilical cord vein endothelial cells were treated with VEGF (476 pM), which induced ACE upregulation. Cotreatment with atorvastatin (0.1–10 μM) dose dependently inhibited VEGF-induced ACE upregulation. In the presence of mevalonate (100 μM), atorvastatin failed to downregulate VEGF-induced ACE production. Cotreatment of the cells with either farnesylpyrophosphate (FPP; 5 μM) or geranylgeranylpyrophosphate (GGPP; 5 μM) partially inhibited the suppressive effect of atorvastatin. Pretreatment of the cells with Rho-associated protein kinase inhibitor, Y-27632 (10 μM), partially inhibited VEGF-induced ACE upregulation. VEGF (476 pM) caused PKC phosphorylation, which was inhibited by cotreatment of the cells with atorvastatin. Atorvastatin inhibited VEGF-induced ACE upregulation probably by inhibiting PKC phosphorylation. This effect was mediated via inhibition of the mevalonate pathway. ACE downregulation may be an additional beneficial effect of statins in the treatment of cardiovascular disease.

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