Is maternal intake of ALA from Flaxseed neuroprotective against neonatal hypoxicischemic brain injury?

Brain injury due to hypoxiaischemia (HI) is a major cause of neonatal morbidity and mortality. n3 PUFA, especially DHA, seem to exert neuroprotection. Flaxseed (Linum usitatissimum) is rich in ALA, DHA’s precursor. This study aims to investigate the possible neuroprotective effect of maternal flaxseed intake on the offspring submitted to HI. Wistar dams were divided in 2 groups: flaxseed (F) or soy oil (Control  C). The experimental diets were fed to dams during pregnancy and lactation; standard diet was given to postweaning pups. Male pups were separated in 3 subgroups within each dietary group on postnatal day (P) 7: HI (CHI and FHI), in which pups underwent HI protocol according to Vannucci et al. (1999); Sham (CSh and FSh), the false surgery group; Control (CC and FC). The pups’ hippocampal FA composition was analysed at weaning. From P30 to P50, animals were subjected to Tail Suspension (TS) and Forced Swimming (FS) tests, to evaluate depressive behavior, and Morris Water Maze (MWM), to access spatial memory. At P60, the animals' brains were removed and weighted. Hippocampus from F group presented lower n6 PUFA and n6 ri n3 ratio and higher MUFA and n3 PUFA, including DHA. Immobility in TS test was lower in CHI than CC and CSh and in F groups compared to C groups. Concerning FS, immobility, climbing and swimming parameters showed decreased depression like behavior in both HI groups and in F groups compared to C counterparts. CHI presented higher latency period to find the hidden platform than CC and CSh in days 3, 4 and 14. FHI presented higher brain weight than CHI. The results suggest that maternal flaxseed intake changes offspring’s hippocampal FA profile, promoting DHA accretion; both HI and flaxseed showed antidepressive effects; flaxseed prevented spatial memory impairment and reduced brain tissue loss caused by HI. (Authors abstract)