EFFECTS OF STATINS AND OTHER BIOLOGICAL PREPARATIONS UPON ACTIVATION OF MITOGEN-ACTIVATED PROTEIN KINASES IN PATIENTS WITH RHEUMATOID ARTHRITIS

Abstract. In this study, we evaluated effects of statins and other biological preparations upon spontaneous and stimulated activation of МАРК p38 and ERK1/2 in monocytes from the patients with rheumatoid arthritis (RA). We used peripheral blood mononuclear cells (PBMC) from RA patients and healthy d...

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Autores principales: I. V. Shirinsky, V. A. Kozlov, V. S. Shirinsky
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Publicado: SPb RAACI 2014
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spelling oai:doaj.org-article:125341fdbf2044dfa262ffa6d2efc6082021-11-18T08:03:38ZEFFECTS OF STATINS AND OTHER BIOLOGICAL PREPARATIONS UPON ACTIVATION OF MITOGEN-ACTIVATED PROTEIN KINASES IN PATIENTS WITH RHEUMATOID ARTHRITIS1563-06252313-741X10.15789/1563-0625-2009-1-71-78https://doaj.org/article/125341fdbf2044dfa262ffa6d2efc6082014-07-01T00:00:00Zhttps://www.mimmun.ru/mimmun/article/view/190https://doaj.org/toc/1563-0625https://doaj.org/toc/2313-741XAbstract. In this study, we evaluated effects of statins and other biological preparations upon spontaneous and stimulated activation of МАРК p38 and ERK1/2 in monocytes from the patients with rheumatoid arthritis (RA). We used peripheral blood mononuclear cells (PBMC) from RA patients and healthy donors. PBMC were cultured in presence of 0, 0.1, 1 or 10 мM mevastatin, 10 мg/ml IL-1 receptor antagonist (IL-1Ra), 5 мg/ml infliximab, and 5 мg/ml soluble pegylated p55 TNF-receptor (r-met-Hu-sTNF-RI). To study the mechanisms of mevastatin effects upon МАРК p38 and ERK1/2 activities, L-mevalonate was added to the cultures. The cells were stained with anti-phospho-MAPK p38, or anti-phospho-ERK1/2, and analyzed with flow cytometry. We have shown that IL-1Ra and r-met-Hu-sTNF-RI inhibited spontaneous MAPK р38 activation. Mevastatin reduced spontaneous MAPK p38 and ERK1/2 phosphorylation. Mevastatininduced suppression of MAPK p38 and ERK1/2 activation was not dose-dependent. L-mevalonate completely prevented mevastatin-induced reduction of MAPK р38 phosphorylation and partially reversed inhibition of МАРК ERK1/2. In conclusion, decrease in MAPK activation represents a common mechanism of anti-inflammatory effects exerted by statins and some other biologicals.I. V. ShirinskyV. A. KozlovV. S. ShirinskySPb RAACIarticlerheumatoid arthritismitogen-activated proteinkinasesstatinsbiologicalsImmunologic diseases. AllergyRC581-607RUMedicinskaâ Immunologiâ, Vol 11, Iss 1, Pp 71-78 (2014)
institution DOAJ
collection DOAJ
language RU
topic rheumatoid arthritis
mitogen-activated proteinkinases
statins
biologicals
Immunologic diseases. Allergy
RC581-607
spellingShingle rheumatoid arthritis
mitogen-activated proteinkinases
statins
biologicals
Immunologic diseases. Allergy
RC581-607
I. V. Shirinsky
V. A. Kozlov
V. S. Shirinsky
EFFECTS OF STATINS AND OTHER BIOLOGICAL PREPARATIONS UPON ACTIVATION OF MITOGEN-ACTIVATED PROTEIN KINASES IN PATIENTS WITH RHEUMATOID ARTHRITIS
description Abstract. In this study, we evaluated effects of statins and other biological preparations upon spontaneous and stimulated activation of МАРК p38 and ERK1/2 in monocytes from the patients with rheumatoid arthritis (RA). We used peripheral blood mononuclear cells (PBMC) from RA patients and healthy donors. PBMC were cultured in presence of 0, 0.1, 1 or 10 мM mevastatin, 10 мg/ml IL-1 receptor antagonist (IL-1Ra), 5 мg/ml infliximab, and 5 мg/ml soluble pegylated p55 TNF-receptor (r-met-Hu-sTNF-RI). To study the mechanisms of mevastatin effects upon МАРК p38 and ERK1/2 activities, L-mevalonate was added to the cultures. The cells were stained with anti-phospho-MAPK p38, or anti-phospho-ERK1/2, and analyzed with flow cytometry. We have shown that IL-1Ra and r-met-Hu-sTNF-RI inhibited spontaneous MAPK р38 activation. Mevastatin reduced spontaneous MAPK p38 and ERK1/2 phosphorylation. Mevastatininduced suppression of MAPK p38 and ERK1/2 activation was not dose-dependent. L-mevalonate completely prevented mevastatin-induced reduction of MAPK р38 phosphorylation and partially reversed inhibition of МАРК ERK1/2. In conclusion, decrease in MAPK activation represents a common mechanism of anti-inflammatory effects exerted by statins and some other biologicals.
format article
author I. V. Shirinsky
V. A. Kozlov
V. S. Shirinsky
author_facet I. V. Shirinsky
V. A. Kozlov
V. S. Shirinsky
author_sort I. V. Shirinsky
title EFFECTS OF STATINS AND OTHER BIOLOGICAL PREPARATIONS UPON ACTIVATION OF MITOGEN-ACTIVATED PROTEIN KINASES IN PATIENTS WITH RHEUMATOID ARTHRITIS
title_short EFFECTS OF STATINS AND OTHER BIOLOGICAL PREPARATIONS UPON ACTIVATION OF MITOGEN-ACTIVATED PROTEIN KINASES IN PATIENTS WITH RHEUMATOID ARTHRITIS
title_full EFFECTS OF STATINS AND OTHER BIOLOGICAL PREPARATIONS UPON ACTIVATION OF MITOGEN-ACTIVATED PROTEIN KINASES IN PATIENTS WITH RHEUMATOID ARTHRITIS
title_fullStr EFFECTS OF STATINS AND OTHER BIOLOGICAL PREPARATIONS UPON ACTIVATION OF MITOGEN-ACTIVATED PROTEIN KINASES IN PATIENTS WITH RHEUMATOID ARTHRITIS
title_full_unstemmed EFFECTS OF STATINS AND OTHER BIOLOGICAL PREPARATIONS UPON ACTIVATION OF MITOGEN-ACTIVATED PROTEIN KINASES IN PATIENTS WITH RHEUMATOID ARTHRITIS
title_sort effects of statins and other biological preparations upon activation of mitogen-activated protein kinases in patients with rheumatoid arthritis
publisher SPb RAACI
publishDate 2014
url https://doaj.org/article/125341fdbf2044dfa262ffa6d2efc608
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AT vakozlov effectsofstatinsandotherbiologicalpreparationsuponactivationofmitogenactivatedproteinkinasesinpatientswithrheumatoidarthritis
AT vsshirinsky effectsofstatinsandotherbiologicalpreparationsuponactivationofmitogenactivatedproteinkinasesinpatientswithrheumatoidarthritis
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