Аннотация:Introduction: The aim of the study was to evaluate the effect of xenon
on the activation of human neutrophils in ex vivo conditions.
Methods: After receiving informed consent, 10 healthy volunteers had
their blood drawn twice: before xenon inhalation (xenon - 30 vol.%,
oxygen - no more than 40 vol.%, the rest - nitrogen) and immedi-
ately after. The duration of inhalation in all patients was 60 min. After neutrophil isolation from the patient’s serum, lipopolysaccharide (LPS)
was added to the 4 million/ml cell concentrate at a dose of 200 ng/ml.
The effect of xenon on the severity of inflammatory activation of neu-
trophils was assessed by the level of expression of CD11b and CD66b
adhesion molecules on their surface and phosphorylation of pro-
inflammatory kinases: ERK1/2 and kinase-p38.
Results: The addition of lipopolysaccharide to the neutrophil incu-
bation medium caused their activation, significantly increasing the
phosphorylation of the key pro-inflammatory kinases of neutrophils:
ERK1/2 and kinase-p38. After xenon anesthesia, there was a decrease
in the expression of CD11b and CD66b adhesion molecules on the
neutrophil surface and reducing the phosphorylation (activation) of
pro-inflammatory kinases: ERK1/2 and MAP-kinase p38, which dem-
onstrated its anti-inflammatory effect. The addition of LPS to the
neutrophil incubation medium reduced their ability to spontaneous
apoptosis 22 h after isolation, which was 22.6%, which was 60% less
than in the control group-56.3% (p < 0.05). Xenon inhalation signifi-
cantly increased to 41.35% (p < 0.05) the ability of neutrophils to spon-
taneous apoptosis after incubation with LPS.
Conclusions: Inhalation of xenon 30 vol% for 60 min has a pro-
nounced anti-inflammatory effect on neutrophils, reducing their acti-
vation by inhibiting pro-inflammatory kinases: ERK1/2 and MAP-kinase
p38, reducing the expression of activation markers CD11b and CD66b
on the surface of neutrophils and increasing their ability to spontane-
ous apoptosis.