Neuroprotective effects of TSA against oxygen-glucose deprivation in SH-SY5Y cells

Aim To investigate the protective effects of histone deacetylase inhibitor(HDACi),trichostatin A(TSA),on oxygen-glucose deprivation(OGD) in SH-SY5Y cells and the underlying mechanism.Methods SH-SY5Y cells were cultured with DMEM medium,OGD model was established and evaluated based on cell viability.Afterwards,the influences of TSA(10,20,40 and 80 nmol·L-1) treatment on the neuron injury induced by OGD were analyzed,morphological changes were observed with inverted microscope,cell viability was measured by methyl thiazolyl tetrazolium(MTT) assay,cell apoptosis and necrosis were detected by PI and Hoechst staining,the level of intracellular reactive oxygen species(ROS) and potential of mitochondrial membrane(MMP) were evaluated by Fluorescence microscope.Results Oxygen-glucose deprivation for 2 hours significantly suppressed the cell viability and MMP of SH-SY5Y,the intracellular level of ROS increased obviously.Moreover,the number of apoptotic and necrotic cells increased as the extending of oxygen-glucose deprivation.Compared with OGD group,40 nmol·L-1TSA significantly improved cellular viability and MMP,reduced intracellular ROS.Conclusion These data demonstrate the neuroprotective effects of TSA on OGD induced injury in SH-SY5Y cells,the underlying mechanisms may partially be due to the effects of TSA on an anti-oxidative stress,and maintaining of mitochondria function.