THE ROLE OF REDOX-DEPENDENT SIGNAL SYSTEMS IN THE REGULATION OF APOPTOSIS UNDER OXIDATIVE STRESS CONDITION
N. V. Ryazanceva, V. V. Novickiy, N. Yu. Chasovskih,1 E. V. Kaigorodova, E. G. Starikova, U. V. Starikov, T. T. Radzivil, I. V. Krat
Siberian State Medical University, Tomsk;
1 e-mail: cnil.@mail.ru
Programmed death of peripheral blood mononuclear cells from donors with acute inflammatory diseases (an acute appendicitis, a community-acquired
pneumonia) was investigated under condition of oxidative stress in vitro and under effect of selective inhibitors of MAP-kinases JNK and p38. Levels of active and
inactive forms of MAP-kinases, and factors of transcription were determined by immunoblotting (western blot analysis). The increase in the activity of apoptosis
under condition of oxidative stress in vivo and during the acute inflammatory diseases is associated with the increase in the level of reactive oxygen species
(ROS) in the cells. The action of inhibitors of MAP-kinases JNK (SP600125) and p38 (ML3403) in vitro under condition of oxidative stress prevents increase in the
quantity of annexin-positive mononuclear leucocytes that testifies to involving JNK and p38 MAP-kinases in apoptosis deregulation oxidative mechanisms.
The appearance of NF-eB in the mononuclear leucocytes under condition of oxidative stress during the acute inflammatory diseases and at the experiment was
shown; p53 was registered only under condition of oxidative stress in vitro. The effect of p53 and NF-eB results in the increase in the quantity of apoptosis
annexin-positive mononuclear leucocytes that testify to inoperativeness of antiapoptotic regulation NF-eB.
Key words: oxidative stress, acute inflammation, ROS, apoptosis, mitogen-activated protein kinases JNK, p38, p53, NF-eB
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