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

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.