Nꭃ-nitro-l-arginine methyl model of pre-eclampsia elicits differential IBA1 and EAAT1 expressions in brain.

Pre-eclampsia (PE) is a pregnancy syndrome associated with an increased risk of both the mother and the baby developing cardiovascular disorders later in life. It is widely accepted that women with severe PE develop a neurological impairment however studies have revealed that the mother and baby are at jeopardy for a neurological deficit later in life. The present study examined expression of Ionized calcium binding adaptor molecule 1 (IBA1) and Excitatory amino acid transporter 1 (EAAT1) as neuroinflammatory markers in an Nꭃ-nitro-l-arginine methyl (L-NAME) model of early- and late-onset (EOPE/ LOPE) PE-like syndrome in rat models. Forty-five adult nulliparous pregnant Sprague-Dawley rats were used for this experiment. They were divided into Control, EOPE and LOPE groups. Administration of L-Name was done between gestational days 8-17 for the treated groups. Animals were sacrificed at gestational day (GD) 19, post-natal day (PND) 1 and 60 and the brain excised for further analysis. Our study confirmed L-NAME induced PE-like symptoms in rat models as evidenced by significant increase in systolic blood pressure and urine protein compared with Control. There was upregulation of IBA1 expression and increased microglial activation in the brain of PE rat models assessed at gestational day 19, post-natal day 1 and 60. Also, IBA1 expression is up regulated in the pups at post-natal day 1 and 60. Contrastingly, EAAT1 expression is down-regulated in the brain of PE rat models assessed at gestational day 19, post-natal day 1 and 60, as well as offspring at post-natal day 1 and 60. These results demonstrate likely neuro-inflammation within the brain of PE mothers during pregnancy, that persist into later life, as well as possible neuro-inflammation in brains of offspring of PE mothers.

Sub-acute nickel exposure impairs behavior, alters neuronal microarchitecture, and induces oxidative stress in rats' brain.

Nickel (Ni) is a heavy metal with wide industrial uses. Environmental and occupational exposures to Ni are potential risk factors for neurological symptoms in humans. The present study investigated the behavior and histomorphological alterations in brain of rats sub-acutely exposed to nickel chloride (NiCl2) and the possible involvement of oxidative stress. Rats were administered with 5, 10 or 20 mg/kg NiCl2 via intraperitoneal injections for 21 days. Neurobehavioral assessment was performed using the Y-maze and open field test (OFT). Histomorphological analyses of brain tissues, as well as biochemical determination of oxidative stress levels were performed. Results showed that Ni treatments significantly reduced body weight and food intake. Cognitive and motor behaviors on the Y-maze and OFT, respectively, were compromised following Ni treatments. Administration of Ni affected neuronal morphology in the brain and significantly reduced percentage of intact neurons in both hippocampus and striatum. Additionally, markers of oxidative stress levels and nitric oxide (NO) levels were significantly altered following Ni treatments. These data suggest that compromised behavior and brain histomorphology following Ni exposures is associated with increase in oxidative stress.