Departamento de Nutrición y Bioquímica, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá D.C., Colombia.
Departamento de Ciencias Clínicas, Facultad de Ciencias de la Salud, Universidad del Tolima, Ibagué, Colombia.
Mol Neurobiol. 2018 Jul;55(7):5462-5477. doi: 10.1007/s12035-017-0777-y. Epub 2017 Sep 25.
High concentrations of palmitic acid in plasma increase both the inflammation associated with obesity and the susceptibility to develop a neurodegenerative event. In the brain, the inflammatory response is mediated by activated microglial cells, which undergo morphological and biochemical changes and can directly affect cell viability. Recent evidence shows that the use of estrogenic compounds can control microglia-induced inflammation with promising results. In this study, we explored the actions of the synthetic steroid tibolone on BV-2 microglia cells stimulated with palmitic acid. Our results demonstrated that tibolone increased cell viability and reduced nuclear fragmentation and the production of reactive oxygen species, as well as preserved mitochondrial membrane potential. These effects were accompanied by reduced nuclear translocation of NF-κB p65, upregulation of neuroglobin, and improved antioxidant defense. Furthermore, estrogen receptor beta (ERβ) inhibition partially dampened tibolone's protective actions in BV-2 cells stimulated with palmitic acid. In conclusion, tibolone protects BV-2 cells by a mechanism involving ERβ and upregulation of neuroglobin.
血浆中高浓度的棕榈酸会增加与肥胖相关的炎症和发生神经退行性事件的易感性。在大脑中，炎症反应是由激活的小胶质细胞介导的，小胶质细胞发生形态和生化变化，并可直接影响细胞活力。最近的证据表明，使用雌激素化合物可以控制小胶质细胞诱导的炎症，并取得了有希望的结果。在这项研究中，我们探讨了合成类固醇替勃龙对棕榈酸刺激的 BV-2 小胶质细胞的作用。我们的结果表明，替勃龙增加了细胞活力，减少了核片段化和活性氧的产生，并保持了线粒体膜电位。这些作用伴随着核内 NF-κB p65 易位减少、神经球蛋白上调和抗氧化防御改善。此外，雌激素受体β（ERβ）抑制部分减弱了替勃龙对棕榈酸刺激的 BV-2 细胞的保护作用。总之，替勃龙通过涉及 ERβ和神经球蛋白上调的机制来保护 BV-2 细胞。
