| Summary: | Objective To investigate the effect of vitamin A (VA) deficiency on lung injury in meconium aspiration syndrome (MAS) in newborn rats. Methods After pregnant rats were fed with normal and deficient VA diet, 25 VA-deficient (VAD) and 25 VA-normal (VAN) neonatal SD rats (7 days old) were obtained, respectively. These rats were used to establish MAS mode. The results of blood gas analysis and wet/dry mass ratio of lung tissue were recorded, compared and analyzed in each group. HE staining was employed to evaluate lung tissue injury. The contents of SP-A protein, SP-C protein, IL-6, vascular endothelial growth factor (VEGF) and tumor necrosis factor-α (TNF-α) in lung tissue were detected by ELISA. β-alanine and other metabolites in the lung tissue was measured with high performance liquid chromatography (HPLC). Results The pH value (P=0.003) and base excess (BE) (P=0.019) were significantly lower in the newborn rats from the VAD group than the VAN group. The VAD group had obviously higher partial pressure of carbon dioxide (PCO2) (P=0.049), wet/dry mass ratio of lung tissue (P=0.001), and contents of IL-6 (P=0.002), VEGF (P=0.003) and TNF-α (P=0.019) than the VAD group, suggesting more serious lung inflammation in the VAD group. Further metabolomic analysis showed that the major signaling pathways between VAD and VAN groups included β-alanine metabolism, cGMP-PKG signaling pathway, olfactory transduction pathway, and neural active ligand-receptor interaction pathway. The result of HPLC indicated that β-alanine was notably up-regulated in rats from the VAD group than the VAN group (P=0.000). Conclusion VAD can aggravate lung injury by up-regulating MAS inflammatory factors, which may be related to the changes in β-alanine metabolic pathways caused by VAD.
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