The interaction between oxidative stress and mast cell activation plays a role in acute lung injuries induced by intestinal ischemia-reperfusion.

BACKGROUND

Both oxidative stress and mast cells are involved in acute lung injuries (ALIs) that are induced by intestinal ischemia-reperfusion (IIR). The aim of this study was to further investigate the interaction between oxidative stress and mast cells during the process of IIR-induced ALI.

MATERIALS AND

METHODS

Thirty adult Sprague-Dawley rats were randomly divided into five groups: sham, IIR, IIR + compound 48/80 (CP), N-acetylcysteine (NAC) + IIR, and NAC + IIR + CP. All rats except those in the sham group were subjected to 75 min of superior mesenteric artery occlusion, followed by 2 h of reperfusion. The rats in the NAC + IIR and NAC + IIR + CP groups were injected intraperitoneally with NAC (0.5 g/kg) for three successive days before undergoing IIR. The rats in the IIR + CP and NAC + IIR + CP groups were treated with CP (0.75 mg/kg), which was administered intravenously 5 min before the reperfusion. At the end of the experiment, lung tissue was obtained for pathologic and biochemical assays.

RESULTS

IIR resulted in ALI, which was detected by elevated pathology scores, a higher lung wet-to-dry ratio, and decreased expression of prosurfactant protein C (P < 0.05). Concomitant elevations were observed in the expression levels of the nicotinamide adenine dinucleotide phosphate oxidase subunits p47(phox) and gp91(phox) and the levels of hydrogen peroxide and malondialdehyde. However, superoxide dismutase activity in the lung was reduced (P < 0.05). The level of interleukin 6, the activity of myeloperoxidase, and the expression of intercellular adhesion molecule 1 were also increased in the lung. IIR led to pulmonary mast cell degranulation and increases in the plasma and pulmonary β-hexosaminidase levels, mast cell counts, and tryptase expression in lung tissue. CP aggravated these conditions, altering the measurements further, whereas NAC attenuated the IIR-induced ALI and all biochemical changes (P < 0.05). However, CP abolished some of the protective effects of NAC.

CONCLUSIONS

Oxidative stress and mast cells interact with each other and promote IIR-induced ALI.