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Background Epigenetic mechanisms such as post-translational histone acetylation are increasingly recognized for their contribution to gene activation and silencing in the brain and contribute to neurodegeneration. Acetylation degree of histones is highly regulated by the enzymes known as histone acetyltransferases (HATs) or histone deacetylases (HDACs). HDAC inhibition affects the expression of only a small subset of genes, leading to transcriptional activation or repression through hyperacetylation of histone or non-histone proteins. HDAC inhibitors are a class of compounds that interfere with the function of HDAC and have been viewed as promising agents to combat neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). Multiple mechanisms underlying the effects of HDAC inhibitors on neuroprotection and restoration of memory and motor impairments in AD or PD models have been proposed, however, little is known about the contribution of HDAC inhibition in glial cells. It has been reported that valproic acid (VPA), a drug commonly used for epilepsy and bipolar disorders, upregulates the expression of neurotrophic factors, including glial cell line-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF) in astrocytes, which contributes to VPAmediated neurotrophic effect on dopamine neurons. VPA also induces microglia apoptosis and suppresses the production of proinflammatory factors in microglia. As VPA is a HDAC inhibitor, we hypothesize that HDAC inhibition may contribute to neuroprotection through regulating gene expressions in glial cells. Materials and methods We thus investigated the effects of several HDAC inhibitors including VPA, trichostatin (TSA), sodium phenylbutyrate (4-PBA) and nicotinamide, on neurotrophic and proinflammatory functions of astrocytes and microglia.

Histone deacetylase inhibition leads to neuroprotection through regulation on glial function