Biological effects of Vitamin E on BV-2 microglial cells

Neuroinflammation is a protective mechanism designed to sustain the brain in response to inflammatory stimuli, however a prolonged inflammatory status, as well as oxidative stress, creates an environment that promotes the onset and progression of neurodegenerative disorders. Microglial cells are responsible for the defence and homeostasis of the Central Nervous System (CSN) and are activated in response to inflammatory stimuli they are commonly referred to as ‘brain resident macrophages’. The pathogenesis of several neurodegenerative diseases is closely linked to the persistent activation of microglia, due to their fundamental role as mediators of inflammation in the brain. The present study is designed to investigate the biological effects of Vitamin E on BV-2 microglia as a potential neuroprotective and anti-inflammatory agent following stimulation with lipopolysaccharide (LPS). Vitamin E represents a family of lipid-soluble compounds consisting of four tocopherols and four tocotrienol derivatives. Vitamin E has both anti-inflammatory and antioxidant properties on CSN, although its neuroprotective effects are clear, the underlying molecular mechanisms remain to be elucidated. Results show that pre-incubation of microglia with vitamin E has neuroprotective effects on LPS-induced microglial activation, preserving the branching morphology typical of microglia in a physiological state, reducing the migratory capacity, the production of pro- and anti-inflammatory cytokines such as TNF-α and IL-10, and finally the activation of receptors such as TRL4 and CD40, which modulate the PI3K-Akt signalling pathway. These results require further understanding and research. However, they open up new future scenarios for the use of vitamin E as an antioxidant to provide greater neuroprotection in vivo for the prevention of possible neurodegenerative diseases.