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![Glutaminase activity inhibition of a DON [μM] and b Gln-VPA [mM] to measure their IC50 values](publication/340897318/figure/fig4/AS:961897935405072@1606345747735/Glutaminase-activity-inhibition-of-a-DON-mM-and-b-Gln-VPA-mM-to-measure-their-IC50.png)
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![Glutaminase activity inhibition of a DON [μM] and b Gln-VPA [mM] to...](publication/340897318/figure/fig4/AS:961897935405072@1606345747735/Glutaminase-activity-inhibition-of-a-DON-mM-and-b-Gln-VPA-mM-to-measure-their-IC50_Q320.jpg)
Glutaminase plays an important role in carcinogenesis and cancer cell growth. This biological target is interesting against cancer cells. Therefore, in this work, in silico [docking and molecular dynamics (MD) simulations] and in vitro methods (antiproliferative and LC–MS metabolomics) were employed to assay a hybrid compound derived from glutamine...
Citations
Blood-brain barrier (BBB) prevents drug access and impedes therapeutic efficacy. Effective methods of modulating barrier function and resolving these difficulties are desperately needed. We hypothesized that cell metabolic adaptation significantly influences physiological and pathological barrier functionality because we were convinced that a better understanding of cell-oriented BBB responses could provide valuable insight, and because metabolic dysregulation is prominent in many vascular-related pathological processes associated with BBB disruption. Biochemical fingerprints of primary brain endothelial cells (EC) were obtained using untargeted liquid chromatography–mass spectrometry (LC-MS) metabolomic profiling during chlorpromazine treatment, at concentration similar to its measured in the serum of high dosed patients, providing a functional readout of cell status. Metabolomic analyses showed brain EC had a distinct metabolic signature. Corroborating their role in BBB and CNS protection. Surprisingly, EC largely maintained their normoxic characteristics in drug treatment situations and their profiles diverged from those of control. When examining EC reactions, tissue specificity/origin is definitely significant. With a focus on cellular metabolism, we examine how cell metabolic adaptive capabilities may influence vascular stability, as well as the prospect that modifying metabolite levels may be an efficient strategy to modulate brain EC function. Overall, this study sheds new light on cell-associated metabolic changes and serves as a valuable resource for understanding BBB modifications in drug treatment circumstances.
