N and subsequent increases in glutathione synthesis [32] brought on by enhanced NADH oxidation [8]. As regards migratory capacity, in some studiesInt. J. Mol. Sci. 2023, 24, x FOR PEER REVIEW7 ofInt. J. Mol. Sci. 2023, 24,like cytokines IL-1, TNF-, ROS, iNOS and COX-2 [46]. BHB suppresses LPS-induced inflammation in BV2 cells by inhibiting NF-B activation and subsequent increases in7gluof 12 tathione synthesis [32] caused by improved NADH oxidation [8]. As regards migratory capacity, in some studies within the literature it has been hypothesized that cells stimulated by LPS undergo improved levels of proinflammatory cytokines and/or AKT/STAT3 sigin the literature it has been hypothesized that cells stimulated by LPS undergo improved naling, when, on the contrary, antioxidant compounds, like BHB, on account of their levels of proinflammatory cytokines and/or AKT/STAT3 signaling, even though, on the contrary, anti-inflammatory effects, strongly inhibit LPS-induced BV2 cell migration by inhibiting antioxidant compounds, including BHB, on account of their anti-inflammatory effects, NF-B/STAT3, as summarized in Figure 5 [74]. Additionally, other research have sugstrongly inhibit LPS-induced BV2 cell migration by inhibiting NF-B/STAT3, as summagested, as among the possible molecular mechanisms involved in neuroprotection, that rized in Figure five [74]. Moreover, other studies have recommended, as one of the probable BHB is capable of modulating dopaminergic neurons by inhibiting LPS-induced micromolecular mechanisms involved in neuroprotection, that BHB is capable of modulating glial activation, each in vitro and in vivo, by mediating the GPR109A signaling pathway dopaminergic neurons by inhibiting LPS-induced microglial activation, both in vitro and [74]. Despite the fact that the molecular mechanisms are still to become explored, it can be deduced, as in vivo, by mediating the GPR109A signaling pathway [74]. While the molecular mechone on the final results of this study, that BHB, and consequently indirectly the ketogenic eating plan, which has anisms are nonetheless to become explored, it could be deduced, as among the list of final results of this study, therapeutic prospective against neurodegenerativehas therapeutic potential against mentioned, altpathologies. That possessing been neurodeBHB, and for that reason indirectly the ketogenic diet program, hough it was confirmedThat having beenthe cellular baseswas confirmed with respect to generative pathologies. with respect to stated, while it involved in neuroprotection mechanisms that involved intherapeutic function in microglial that BHB has a therapeutic role the cellular bases BHB features a neuroprotection mechanisms cells, this becoming a preliminary study, furthercells, thisare needed to provide additional insight in to the necessary to provide in microglial research being a preliminary study, additional studies are molecular mechanisms involved.Honokiol Autophagy additional insight into the molecular mechanisms involved.Lithium dodecyl Epigenetic Reader Domain NeuroinflammationIL-4 IL-13 TGF-NeuroprotectionKETOGENIC DIETIL-6 TNF- Il-1 Reactive MicrogliaLipolysisHomeostatic MicrogliaFFA Acetyl-CoABar: 75HBBar: 75M1 phenotypeM2 phenotypeHBBar: 100HBBar: 100Higher migration capacity IL-10 IL-Lower migration capacity IL-17 IL-HBFigure five.PMID:24455443 The main mechanism of ketogenic diet plan action on microglia via BHB production. Figure 5. The key mechanism of ketogenic diet plan action on microglia by means of BHB production.four. Supplies and Approaches four. Components and Strategies 4.1. Cell Culture and Remedy 4.1. Cell Culture and Therapy The immortalized mouse microglia.
