The medial septum/diagonal band (MS/DB) is a relay region connecting the hypothalamus and brainstem with the hippocampus, and both the MS/DB and dorsal/ventral hippocampus receive strong topographic GABA/peptidergic projections from the nucleus incertus of the pontine tegmentum. The neuropeptide relaxin-3, released by these neurons, is the cognate ligand for a G i/o -protein-coupled receptor, RXFP3, which is highly expressed within the MS/DB, and both
BackgroundWestern diet and lifestyle are associated with overweight, obesity, and type 2 diabetes, which, in turn, are correlated with neuroinflammation processes. Exercise and a healthy diet are important in the prevention of these disorders. However, molecules inhibiting neuroinflammation might also be efficacious in the prevention and/or treatment of neurological disorders of inflammatory etiology. The abscisic acid (ABA) is a phytohormone involved in hydric-stress responses. This compound is not only found in plants but also in other organisms, including mammals. In rodents, ABA can play a beneficial role in the regulation of peripheral immune response and insulin action. Thus, we hypothesized that chronic ABA administration might exert a protective effect in a model of neuroinflammation induced by high-fat diet (HFD).MethodsMale Wistar rats were fed with standard diet or HFD with or without ABA in the drinking water for 12 weeks. Glucose tolerance test and behavioral paradigms were performed to evaluate the peripheral and central effects of treatments. One-Way ANOVA was performed analyzed statistical differences between groups.ResultsThe HFD induced insulin resistance peripherally and increased the levels of proinflammatory markers in in the brain. We observed that ABA restored glucose tolerance in HFD-fed rats, as expected. In addition, chronic ABA treatment rescued cognitive performance in these animals, while not affecting control diet fed animals. Moreover, it counteracted the changes induced by HFD in the hypothalamus; microglia activations and TNFα mRNA levels.ConclusionThese results suggest that ABA might become a new therapeutic molecule improving the neuroinflammatory status and insulin resistance.
Subjects:The study was conducted on 45 subjects subdivided into three groups: Group I: included 15 patients diagnosed as juvenile myoclonic epilepsy on valproate. Group II: included 15 patients newly diagnosed as juvenile myoclonic epilepsy and didn't receive any antiepileptic treatment before. Group III: included 15 healthy age-and sex-matched volunteers as a control group. Methods: 1-Measurement of serum lncRNA SNHG16 by quantitative real-time reverse transcriptase-polymerase chain reaction (qRT-PCR). 2-Determination of serum 25 OH vitamin D level by ELISA technique.
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