Enteral supplementation of alanyl–glutamine attenuates the up-regulation of beta-defensin-2 protein in lung injury induced by intestinal ischemia reperfusion in rats

• IIR could upregulate the expression of BD-2.
• Glutamine was able to ameliorate IIR-induced injury of remote organs by limiting inflammatory reaction.
• The exact effect of immune-nutrients on BD-2 level in lung after IIR is unknown.
• Its relationship with inflammation and oxidative injury has not been elucidated.
• In IIR animal model, the alteration of BD-2 expression in the lung after oral supplementation of Ala–Gln was investigated.

Background: Beta-defensin-2 (BD-2), an endogenous antimicrobial peptide, plays a key role in immune response against microbial invasion. This study aimed to observe the effect of Alanyl–Glutamine (Ala–Gln) on BD-2 protein expression in pulmonary tissues after intestinal ischemia reperfusion (IIR) in rats and to investigate its correlations to pulmonary inflammatory and oxidative injury. Methods: Rats in IIR and the two treatment groups were subjected to intestine ischemia for 60 min and those in the treatment groups were administered orally with Ala–Gln or alanine (Ala) respectively. Lung tissues were harvested to detect the BD-2 protein expression. Concentrations of Tumor necrosis factor (TNF)-α and malondialdehyde (MDA) as well as superoxide dismutase (SOD) activity in lung tissues were determined simultaneously. Results: Ala–Gln attenuated the up-regulation of BD-2 expression (p < 0.05) and TNF-α (p < 0.05), MDA (p < 0.05) levels, as well as the reduction of SOD activity (p < 0.05) in lung tissues after IIR. But Ala did not exert significant effects. BD-2 protein in lung tissues was positively correlated to local TNF-α level (p < 0.01) and MDA concentration (p < 0.01) with statistical significance. Conclusion: Ala–Gln can relieve the IIR-induced up-regulation of BD-2 protein expression in the lung of rats, which involves anti-inflammation and anti-oxidation mechanisms.