Intestinal ischaemia-reperfusion (I/R) injury can result in
acute lung injury due to ischaemia and
hypoxia.
Dexmedetomidine (Dex), a highly selective alpha2-noradrenergic receptor (α2AR) agonist used in anaesthesia, is reported to regulate
inflammation in organs. This study aimed to investigate the role and mechanism of Dex in
lung injury caused by intestinal I/R. After establishing a rat model of intestinal I/R, we measured the wet-to-dry specific gravity of rat lungs upon treatments with Dex, SB239063 and the α2AR antagonist
Atipamezole. Moreover, injury scoring and histopathological studies of lung tissues were performed, followed by ELISA detection on tumour
necrosis factor-α (TNF-α),
interleukin (IL)-1β and
IL-6 expression. Correlation of
Caveolin-1 (Cav-1)
protein expression with p38, p-p38, p-p65 and p65 in rat lung tissues was analysed, and the degree of cell apoptosis in lung tissues after intestinal I/R injury was detected by TUNEL assay. The
lung injury induced by intestinal I/R was a dynamic process. Moreover, Dex had protective effects against
lung injury by mediating the expression of Cal-1 and α2A -AR. Specifically, Dex promoted Cav-1 expression via α2A -AR activation and mitigated intestinal I/R-induced
lung injury, even in the presence of
Atipamezole. The protective effect of Dex on intestinal I/R-induced
lung injury was also closely related to α2A -AR/
p38 mitogen-activated protein kinases/
nuclear factor-kappaB (MAPK/NF-κB) pathway. Dex can alleviate
pulmonary inflammation after in intestinal I/R by promoting Cav-1 to inhibit the activation of p38 and NF-κB. In conclusion, Dex can reduce pulmonary inflammatory response even after receiving threats from both intestinal I/R injury and
Atipamezole.