Тип публикации: статья из журнала

Год издания: 2008

Идентификатор DOI: 10.1007/s10517-008-0145-z

Ключевые слова: Apoptosis, Mitogen-activated protein kinases, Oxidative stress, Reactive oxygen species, annexin, anthra[1,9 cd]pyrazol 6(2h) one, hydrogen peroxide, mitogen activated protein kinase p38, mitogen activated protein kinase p38 inhibitor, stress activated protein kinase, adult, article, controlled study, enzyme activity, enzyme inhibition, female, human, human cell, in vitro study, leukocyte count, leukocyte culture, male, molecular mechanics, mononuclear cell, Adolescent, Anthracenes, Humans, Imidazoles, JNK Mitogen-Activated Protein Kinases, Leukocytes, Mononuclear, MAP Kinase Signaling System, Middle Aged, p38 Mitogen-Activated Protein Kinases, Protein Kinase Inhibitors, Pyridines, Recombinant Proteins, Young Adult

Аннотация: Programmed death of peripheral blood mononuclear cells from healthy donors was studied during culturing with various concentrations of H2O2 and selective inhibitors of JNK (SP600125) and p38 MAPK (ML3403). In vitro incubation of mononuclear leukocytes with 1 mM H2O2 stimulated apoptotic cell death. Treatment with inhibitors (SP6001Показать полностью25 and ML3403) during in vitro oxidative stress prevented the increase in the number of annexin-positive mononuclear cells. Our results indicate that MAP kinases JNK and p38 are involved in the mechanisms of oxidative dysregulation of apoptosis. © Springer Science+Business Media, Inc. 2008.

Журнал: Bulletin of Experimental Biology and Medicine

Выпуск журнала: Vol. 145, Is. 5

Номера страниц: 569-572

• Ryazantseva N.V. (Department of Pathophysiology, Siberian State Medical University, Federal Agency of Health Care and Social Development, Tomsk, Russian Federation, Department for Fundamental Bases of Clinical Medicine, Siberian State Medical University,)
• Novitsky V.V. (Department of Pathophysiology, Siberian State Medical University, Federal Agency of Health Care and Social Development, Tomsk, Russian Federation, Department for Fundamental Bases of Clinical Medicine, Siberian State Medical University, Fe)
• Chasovskih N.Yu. (Department of Pathophysiology, Siberian State Medical University, Federal Agency of Health Care and Social Development, Tomsk, Russian Federation, Department for Fundamental Bases of Clinical Medicine, Siberian State Medical University,)
• Kaygorodova E.V. (Department of Pathophysiology, Siberian State Medical University, Federal Agency of Health Care and Social Development, Tomsk, Russian Federation, Department for Fundamental Bases of Clinical Medicine, Siberian State Medical University,)
• Starikova E.G. (Department of Pathophysiology, Siberian State Medical University, Federal Agency of Health Care and Social Development, Tomsk, Russian Federation, Department for Fundamental Bases of Clinical Medicine, Siberian State Medical University, F)
• Starikov Yu.V. (Department of Pathophysiology, Siberian State Medical University, Federal Agency of Health Care and Social Development, Tomsk, Russian Federation, Department for Fundamental Bases of Clinical Medicine, Siberian State Medical University, F)
• Radzivil T.T. (Department of Pathophysiology, Siberian State Medical University, Federal Agency of Health Care and Social Development, Tomsk, Russian Federation, Department for Fundamental Bases of Clinical Medicine, Siberian State Medical University, Fe)

• Scopus