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Objective:To explore the effects of histone deacetylase 6(HDAC-6) on the PD cell model induced by proteasome inhibitor lactacystin.Methods:Human neuroblastoma SK-N-SH cells were cultured.The wild type pcDNA3.1-alpha-synuclein eukaryotic expression plasmid was transferred into the cells which then were divided into control group,group L,group T and group T+L.The eells of group L were added with 5 umol/L lactacystin dissolved in dimethylsulfoxide(DMSO) to induce PD cell model with abnormal protein aggregation,the cells of control group were treated with 5 umol/L DMSO,the cells of group T were treated with 5 umol/L selective HDAC-6 inhibitor tubacin dissolved in DMSO,and the cells of group T+L were treated with 5 umol/L lactaeystin and 10 umol/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-synuclein 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 alphasynuclein oligomers can be improved and the cell survival rate can be reduced by the PD cell model induced by lactacystin and treated with selective HDAC-6 inhibitor tubacin,which means that alpha-synuclein 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.
Objective: To explore the effects of histone deacetylase 6 (HDAC-6) on the PD cell model induced by proteasome inhibitor lactacystin. Methods: Human neuroblastoma SK-N-SH cells were cultured. Wild type pcDNA3.1-alpha-synuclein eukaryotic The plasmid was transferred into the cells which then were divided into control group, group L, group T and group T + L. The eells of group L were added with 5 umol / L lactacystin dissolved in dimethylsulfoxide (DMSO) to induce PD cell model with abnormal protein aggregation, the cells of control group were treated with 5 umol / L DMSO, the cells of group T were treated with 5 umol / L selective HDAC-6 inhibitor tubacin dissolved in DMSO, and the cells of group T + L were treated with 5 umol / L lactaeystin and 10 umol / 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 were detected by MTT colorimetric assay, and compared 24 h after the cells were 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-synuclein 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 rates (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 substantially significant (P> 0.05) .Conclusions: The expression level of alphasynuclein oligomers can be improved by the cell survival rate can be reduced by the PD cell model induced by lactacystin and treated with selective HDAC-6 inhibitor tubacin, which means that alpha-synuclein oligomers of the PD cell model induced by lactacystin can be inhibited and the cell survival rate can beimproved by HDAC-6, and the mechanism may be related to the increased of HSP-27 and HSP-70.