Abstract
Experiments on random-bred albino mice showed that application of β2ARs agonist (hexaprenaline sulfate, 1,5 μg/kg, a single dose) and α7nAChRs agonist (GTS-21, 15 mg/kg, a single dose) cause a significant decrease in the mortality of mice from experimental sepsis (i.p., E. coli O157:H7) when it is modeling 2h after using these drugs due to a decrease of the concentration of proinflammatory cytokines TNF-α, IL-1β, and IL-6 (implementation of the cholinergic anti-inflammatory pathway).
Highlights
Mortality from sepsis, depending on various factors, ranges from 12 to 60% of all deaths associated with diseases and their complications [1], and there is an increase in the number of cases of sepsis and the mortality rate from it [2]
The study of the cholinergic anti-inflammatory pathway caused by the action of acetylcholine on α7n-acetylcholine receptors (α7nAChRs) cells of the monocyte-macrophage system (MMC), followed by inhibition of the production by the cells of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and reduced mortality from sepsis were devoted hundreds of articles various authors [6,7,8,9,10,11,12,13,14,15]
The use of β2-adrenergic receptors (β2ARs) agonist hexaprenaline sulfate and α7nAChRs agonist (GTS-21), as well as their combination 2 hours before the sepsis modeling, caused a decrease (p
Summary
Mortality from sepsis, depending on various factors, ranges from 12 to 60% of all deaths associated with diseases and their complications [1], and there is an increase in the number of cases of sepsis and the mortality rate from it [2]. Cholinergic stimulation, as we established in 1987 [3] and in subsequent studies, significantly reduces the mortality of albino mice from sepsis caused by intraperitoneal or intrapulmonary administration, respectively of E. coli and P. vulgaris [3,4,5,6,7]. The study of the cholinergic anti-inflammatory pathway caused by the action of acetylcholine on α7n-acetylcholine receptors (α7nAChRs) cells of the monocyte-macrophage system (MMC), followed by inhibition of the production by the cells of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and reduced mortality from sepsis were devoted hundreds of articles various authors [6,7,8,9,10,11,12,13,14,15]. Reduced production of TNF-α, IL-1β, IL-6 (anti-inflammatory effect occurrence) for cholinergic anti-inflammatory pathway is provided kinase JAK2, transcription factor STAT3, NF-κB transcription factor) [8,9,10,11,12,13,14,15,16,17]
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