孕期补充dha对脂多糖所致仔鼠脑组织小胶质细胞活化和il-1β表达影响-effect of dha supplementation during pregnancy on microglia activation and il - 1β expression in brain tissue of offspring rats induced by lipopolysaccharide.docxVIP

brain injury were observed by pathological section with hematoxylin-eosin (HE) staining method.Results Pregnant rats of each group had normal activity and feeding after intraperitoneal injection. In the LPS-treated group, one pregnant rat was dead, one was abortion, and two pregnant rats were premature delivery and a part of their offspring had already dead. The mean birth weight of the rat pups in the LPS-treated group was significant lower than the control group and DHA-treated group (p0.05), the hematoxylin- eosin (HE) stained placenta sections showed remarkable interstitial hyperplasia, narrow capillary and inflammatory infiltration, and brain HE stained sections showed cellular edema, tissue rarities and cell population decreased. In DHA-treated group, only one pregnant rat was abortion, none of them was dead, the placentas showed less inflammatory cells infiltration, and had rich blood supply. The control group showed nothing abnormal. Compared with control group: 1) The IL-1β mRNA expressions in brain tissue were increased remarkably till P14 in LPS-treated group (p0.05), but increased slightly in DHA-treated group till P7 (p0.05). 2) The IL-1β protein secretions were increased remarkably till P14 in LPS-treated group (p0.05), but increased slightly in DHA-treatedgroup before P7 (p0.05). 3）The mRNA expression of MyD88 increased significantly atG21 and P1 in LPS-treated group and DHA-treated group (p0.05). 3) Up to P14, OX42 positive microglias increased constantly in LPS-treated group (p0.05), in DHA-treated group which increased till P7 (p0.05), but there were little diffirence at P14.Conclusions Intraperitoneal LPS (350μg/kg body weight) administration to pregnant rats induced an inflammatory response of placenta and fetus, finally resulted in brain injury. Maternal DHA treatment during pregnancy attenuates LPS-induced intrauterine and fetus brain inflammation by reducing the persistent expression of inflammatory cytokine IL-1β and microglia activation in