Effect of HDAC-6 on PD cell induced by lactacystin

Objective: To explore the effects of histone deacetylase 6 (HDAC-6) on the PI) ccll model induced by protcasome inhibitor lactacystin. Methods: Human neuroblastoma SK-N-SH cells were cultured. The wild type pcDNA3.1-alpha-synuclein eukaryotie expression plasmid was transferred into the cells which then were divided into control group. group L, group T and group T+L. The cells of group L were added with 5 mu mol/l. lactacystin dissolved in dimethylsulfoxide (DMSO) to induce PD cell model with abnormal protein aggregation, the cells of control group were treated with 5 mu mol/L DMSO, the cells of group T were treated with 5 mu mol/L selective HDAC-6 inhibitor tubacin dissolved in DMSO, and the cells of group T+L were treated with 5 mu mol/L lactacystin and 10 mu mol/L tubacin dissolved in DMSO. The expression levels of alpha-synuclein oligomers, HSP-27 and HSP-70 were detected by Western blot and the cell survival rate of all the groups was detected by MTT colorimetric assay. and compared 24 h after the cells were treated. Results: The expression levels of alpha-synuclein oligomers. HSP-27 and HSP-70 of the cells of group L were significantly higher than the control group, and the cell survival rate was significantly lower (P<0.05); the expression level of alpha-synuclcin oligomers of the cells of group T+L was significantly higher than group L. but the expression level of HSP-27 and HSP-70 were significantly lower, and so as the cell survival rate (P<0.05); the differences of the expression level of alpha-synuclein oligomers, HSP-27 and HSP-70 and the cell survival rate of the cells of group T and the control group were not statistically significant (P>0.05). Conclusions: The expression level of alpha-synuclein oligomers can be improved and the cell survival rate can be reduced by the PI) cell model induced by lactacystin and treated with selective HDAC-6 inhibitor tubacin, which means that alpha-synuclcin oligomers of the PD cell model induced by lactacystin can be inhibited and the cell survival rate can be improved by HDAC-6, and the mechanism may be related to the increased of HSP-27 and HSP-70.