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Background The term sepsis is used to designate a systemic condition of infection and inflammation associated with hemodynamic changes that result in organic dysfunction. Gestational sepsis can impair the development of the central nervous system and may promote permanent behavior alterations in the offspring. The aim of our work was to evaluate the effects of maternal sepsis on inflammatory cytokine levels and synaptic proteins in the hippocampus, neocortex, frontal cortex, and cerebellum of neonatal, young, and adult mice. Additionally, we analyzed the motor development, behavioral features, and cognitive impairments in neonatal, young and adult offspring. Methods Pregnant mice at the 14th embryonic day (E14) were intratracheally instilled with saline 0.9% solution (control group) or Klebsiella spp. (3 × 108 CFU) (sepsis group) and started on meropenem after 5 h. The offspring was sacrificed at postnatal day (P) 2, P8, P30, and P60 and samples of liver, lung, and brain were collected for TNF-α, IL-1β, and IL-6 measurements by ELISA. Synaptophysin, PSD95, and β-tubulin levels were analyzed by Western blot. Motor tests were performed at all analyzed ages and behavioral assessments were performed in offspring at P30 and P60. Results Gestational sepsis induces a systemic pro-inflammatory response in neonates at P2 and P8 characterized by an increase in cytokine levels. Maternal sepsis induced systemic downregulation of pro-inflammatory cytokines, while in the hippocampus, neocortex, frontal cortex, and cerebellum an inflammatory response was detected. These changes in the brain immunity were accompanied by a reduction of synaptophysin and PSD95 levels in the hippocampus, neocortex, frontal cortex, and cerebellum, in all ages. Behavioral tests demonstrated motor impairment in neonates, and depressive-like behavior, fear-conditioned memory, and learning impairments in animals at P30 and P60, while spatial memory abilities were affected only at P60, indicating that gestational sepsis not only induces an inflammatory response in neonatal mouse brains, but also affects neurodevelopment, and leads to a plethora of behavioral alterations and cognitive impairments in the offspring. Conclusion These data suggest that maternal sepsis may be causatively related to the development of depression, learning, and memory impairments in the litter.

O AVE hemorrágico é uma das principais causas de morte e incapacidade funcional em todo mundo, sendo este tipo de AVE o mais grave, em comparação com o isquêmico. Considerando a alta mortalidade do AVE hemorrágico e a gravidade das disfunções que permanecem após o quadro hemorrágico, é de grande importância a busca por novas terapias, capazes de diminuir as sequelas motoras decorrentes dos danos encefálicos primários e secundários causados pela hemorragia intracerebral. Sendo assim, este estudo buscou investigar o potencial neuroprotetor dos chás verde e vermelho provenientes da Camellia sinensis (suplementação iniciada 10 dias antes do AVE e mantida até o fim dos testes comportamentais) em um quadro de AVE hemorrágico (mimetizado pela infusão de colagenase intraestriatal) em ratos Wistar machos. Para avaliar a função motora dos animais, foram utilizados os testes de Campo Aberto (CA), Rotarod (RR) e Escala de Déficit Neurológico (EDN). Para avaliar o, o equilíbrio oxidativo estriatal avaliamos a presença de espécies reativas (ER/DCFH), a peroxidação lipídica (TBARS; espécies reativas ao ácido tiobarbitúrico), os níveis de glutationa (GSH) e capacidade antioxidante total (FRAP). Nossos resultados mostraram que o AVE hemorrágico causa dano motor e oxidativo nos ratos (aumento do TBARS), porém não altera os níveis de antioxidantes no tecido estriatal. Além disso, os chás mostraram-se estratégias parcialmente eficazes contra o dano motor e estresse oxidativo. Estes resultados revelam a possibilidade da utilização dos chás verde e vermelho como estratégia de neuroproteção, no entanto estudos adicionais são necessários para que os mecanismos de ação dos dois chás frente ao quadro hemorrágico sejam completamente elucidados. Hemorrhagic stroke is one of the leading causes of death and functional disability worldwide, and this type of stroke is the most severe compared to the ischemic stroke. Considering the high mortality of the hemorrhagic stroke and the severity of the dysfunctions that remain after the hemorrhagic stage, it is important to search for new therapies to reduce the motor sequelae due to primary and secondary brain damage caused by intracerebral hemorrhage. Therefore, this study aimed to investigate the neuroprotective potential of the green and red teas from Camellia sinensis (supplementation started 10 days before the stroke and maintained until the end of the behavioral tests) in a hemorrhagic stroke (mimicked by infusion of intra-striatal collagenase) in male Wistar rats. To evaluate the motor function of the animals, the Open Field (OF), Rotarod (RR) and Neurological Deficit Scale (NDS) tests were used. In order to evaluate the striatal oxidative balance we evaluated the presence of reactive species (RS/DCFH), the lipid peroxidation (TBARS, thiobarbituric acid reactive species), the glutathione levels (GSH), and total antioxidant capacity (FRAP). Our results showed that hemorrhagic stroke causes motor and oxidative damage in rats (increase of TBARS), but does not alter the antioxidant levels in the striatal tissue. In addition, teas showed to be partially effective in avoid motor damage and oxidative stress. These results reveal the possibility of using the green and red teas as a neuroprotection strategy; however, additional studies are necessary so that the mechanisms of action of the two teas in hemorrhagic condition can be elucidated.