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DC Field | Value | Language |
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dc.contributor.author | Bakhtiyar Iriskuov Bakhrom Muinjonov, Behzod Abdullayev Tuychiboy Nishonov Kamila Porsokhonova | - |
dc.date.accessioned | 2019-11-20T12:19:46Z | - |
dc.date.available | 2019-11-20T12:19:46Z | - |
dc.date.issued | 2016-06-24 | - |
dc.identifier.uri | http://repository.tma.uz/xmlui/handle/1/272 | - |
dc.description.abstract | Enhanced leukocyte recruitment is an inflammatory process that occurs during early phases of the vascular dysfunction that characterises atherosclerosis. We evaluated the impact of anti-TNF-α (adali-mumab, infliximab and etanercept) and anti-IL-12/23 (ustekinumab) on interactions between human leukocytes and endothelial cells in a flow chamber that reproduced in vivo conditions. Clinical con-centrations of anti-TNF-α were evaluated on the leukocyte recruitment induced by a variety of en-dothelial (TNF-α, interleukin-1β, lymphotoxin-α and angiotensin-II) and leukocyte (PAF, IL-12 and IL-23) stimuli related to inflammation and atherosclerosis. Treatment with anti-TNF-α, even before or after establishing the inflammatory situation induced by TNF-α, diminished leukocyte–endothelial cell in-teractions induced by this stimuli. Our results also implicated adhesion molecules (ICAM-1, VCAM-1 and E-selectin) in the actions of anti-TNF-α in terms of leukocyte adhesion to endothelium. However, anti-TNF-α drugs did not influence the actions of interleukin-1β, but prevented those of lymphotoxin-α and angiotensin-II. However, once established, inflammatory response elicited by the latter three stimuli could not be reversed. Pre-treatment with anti-TNF-α, also prevented leukocyte actions induced by IL-23 on PBMC rolling flux and rolling velocity and by IL-12 on PMN adhesion. Ustekinumab exhibited a more discreet profile, having no effect on leukocyte recruitment induced by any of the endothelial stimuli, while blocking the effects of IL-23 on leukocyte activation and those of IL-12 on PMN adhesion and PAF on PBMC rolling velocity. These findings endorse the idea that biological anti-inflammatory drugs, in particular anti-TNF-α, have the capacity to influence cardiovascular risk accompanying psoriasis and rheumatoid arthritis by ameliorating vascular inflammation. © 2016 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY license | en_US |
dc.language.iso | en | en_US |
dc.publisher | Tashkent Medical Academy | en_US |
dc.subject | Biologics Anti-TNF-α agents Anti-IL agents Endothelial cell interactions | en_US |
dc.title | Experimental HUVEC expression of adhesion molecules in detecting effects of anti-interleukine agents | en_US |
dc.type | Thesis | en_US |
Appears in Collections: | Thesis, Articles |
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File | Description | Size | Format | |
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Experimental HUVEC expression of adhesion molecules in detecting effects of anti-interleukine agents.pdf | Experimental HUVEC expression of adhesion molecules in detecting effects of anti-interleukine agents | 1.53 MB | Adobe PDF | View/Open |
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