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2015 ; 4
(ä): 800
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The role of spleen in the treatment of experimental lipopolysaccharide-induced
sepsis with dexmedetomidine
#MMPMID26702389
Liu Z
; Wang Y
; Ning Q
; Gong C
; Zhang Y
; Zhang L
; Bu X
; Jing G
Springerplus
2015[]; 4
(ä): 800
PMID26702389
show ga
Dexmedetomidine (Dex), a highly selective ?2-adrenergic receptor agonist, has
been shown to attenuate systemic inflammatory response induced by
lipopolysaccharide (LPS). The protective effects of Dex may reportedly be due to
the activation of the ?7 nicotinic acetylcholine receptor (?7nAChR)-dependent
cholinergic anti-inflammatory pathway. Spleen has been shown to play a pivotal
role in the neural cholinergic anti-inflammatory pathway. However, little is
known about the specific function of spleen in the protective effects of Dex
against sepsis. To investigate the role of spleen in the treatment of Dex against
sepsis, we studied the effects of preemptive administration of Dex to septic mice
on the NF-?B p65 activation and downstream pro-inflammatory cytokine expression
in the spleen. Our results provided evidence that Dex treatment attenuated
LPS-activated NF-?B p65 activation, as well as the production of tumor necrosis
factor-?, interleukin-6, and interleukin-1? at the level of both mRNA and protein
in spleen. Consequently, serum concentrations of these cytokines decreased.
Conversely, preemptive injection of ?-bungarotoxin, a selective ?7nAChR
antagonist, reversed these effects of Dex. Our findings indicated that spleen
played a critical role in the protective effects of Dex against sepsis and
provided further insight into the anti-inflammatory mechanisms of Dex.