| Autor: |
Petrushanko IY; Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, 119991 Russia., Melnikova EV; Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, 119991 Russia., Yurinskaya MM; Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, 119991 Russia.; Institute of Cell Biophysics, Russian Academy of Sciences, Pushchino, Moscow Region, 142290 Russia., Vinokurov MG; Institute of Cell Biophysics, Russian Academy of Sciences, Pushchino, Moscow Region, 142290 Russia., Suslikov AV; Hospital of the Pushchino Research Center, Pushchino, Moscow Region, 142290 Russia., Mitkevich VA; Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, 119991 Russia., Makarov AA; Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, 119991 Russia.; aamakarov@eimb.ru. |
| Abstrakt: |
Lipopolysaccharides (LPS), components of the cell wall of gram-negative bacteria, activate neutrophils that trigger pathological processes, including gram-negative sepsis. LPS inhibit spontaneous apoptosis of neutrophils that leads to inflammation. In this work we tested the action of H2S donor (GYY4137) on the activation of human neutrophils by E. coli LPS. We estimated the changes in redox status (ROS level, intracellularglutathione, NO), apoptosis and mitochondrial potential of neutrophils under the LPS action in the presence and absence of GYY4137. GYY4137 reduces the ROS level, slightly reduces GSH, does not influence the NO level and has no apoptogenic effect. LPS induce the increasing of ROS level and inhibit spontaneous apoptosis of neutrophils. We found that GYY4137 prevents the growth of ROS caused by LPS and leads to a reduction of LPS-induced inhibition of neutrophil apoptosis. Thus the mechanism of GYY4137 protection against inflammation, triggered by bacterial infection, is concerned with the neutralization of LPS effect on neutrophils. |
