Abstract

Background: In rats, in utero exposure to dexamethasone mimics gestational stress and showed reduction in brain weight and myelination. At postnatal day 7 (P7), in vivo 1H-MRS showed alterations of cerebral metabolism in cortex and hippocampus, suggesting impairment of brain structure, energy metabolism and neurotransmitter. Lactoferrin (Lf) an iron-binding glycoprotein secreted in milk with an antioxidant activity is transferred into the the brain after oral administration. Aims: We hypothesized that Lf could influence brain development and prevent cerebral damages following prenatal exposure to glucocorticoids. Methods: Rats were treated with DEX (100 µg/kg/ day) during the third week of gestation with access to standard diet (Ctrl-DEX), or Lactoferrin-enriched diet (1 g/kg/day) during gestation and lactation (Lf-DEX). Sham rats not exposed to DEX fed with standard diet (Ctrl-Veh). In vivo 1H-MRSpectroscopy of hippocampus and cortex were acquired at P7 and compared using a Kruskal-Wallis test. Results: Ctrl-DEX group showed decreased of NAA-NAAG in the hippocampus compared to Ctrl- Veh group (2.55±0.26mM vs 3.37±0.10mM, p< 0.05). A decrease of Glu-Gln was observed in both the hippocampus (3.74±0.85mM vs 5.32±0.66mM, p< 0.05) and the cortex (2.95±0.66mM vs 5.62±0.78mM, p< 0.05). No differences have been found between Lf-DEX group and both Ctrl-Veh and Ctrl-DEX groups. Conclusions: Variation of NAA-NAAG and Glu-Gln, considered as markers of neuronal integrity and function, confirmed the altered brain development after Dex exposure and revealed the potential protective effect of the lactoferrin in a rat model of prenatal exposure to adverse conditions.

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