Propofol prevents lung injury after intestinal ischemia-reperfusion by inhibiting the interaction between mast cell activation and oxidative stress.

Both mast cells and oxidative stress are involved in acute lung injury (ALI) induced by intestinal ischemia-reperfusion (IIR). The aim of this study was to investigate whether propofol could improve IIR-induced ALI through inhibiting their interaction. Repetitive, brief IIR or IIR+compound 48/80 was performed in adult Sprague-Dawley rats pretreated with saline, apocynin or propofol. And their lungs were excised for histology, ELISA and protein-expression measurements 2h after reperfusion. Rats pretreated with saline developed critical ALI 2h after IIR. We found significant elevations in lung injury scores, lung wet/dry ratio and gp91phox, p47phox, intercellular cell adhesion molecule-1 protein expressions and higher level of malondialdehyde, interleukin-6 contents, and myeloperoxidase activities, as well as significant reductions in superoxide dismutase activities, accompanied with increases in mast cell degranulation evidenced by significant increases in mast cell counts, β-hexosaminidase concentrations, and tryptase expression. And the lung injury was aggravated in the presence of compound 48/80. However, pretreated with propofol and apocynin not only ameliorated the IIR-mediated pulmonary changes beyond the biochemical changes but also reversed the changes that were aggravated by compound 48/80. Propofol protects against IIR-mediated ALI, most likely by inhibiting the interaction between oxidative stress and mast cell degranulation.