title: Effect of HDAC-6 on PD cell induced by lactacystin.
abstract: 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 cells of group L were added with 5 μmol/L lactacystin dissolved indimethylsulfoxide (DMSO) to induce PD cell model with abnormal protein aggregation, the cells of control group were treated with 5 μmol/L DMSO, the cells of group T were treated with 5 μmol/L selective HDAC-6 inhibitor tubacin dissolved in DMSO, and the cells of group T+L were treated with 5 μmol/L lactacystin and 10 μmol/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 alpha-synuclein 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.
authors.affiliation: Nanfang Hospital, Southern Medical University, China; Department of Neurology, Inner Mongolia North Heavy Industries Group Corp. Ltd Hospital (The Third Affiliated Hospital of Baotou Medical College), China.
authors.forename: Li-Fei
authors.initials: LF
authors.lastname: Xing
authors.affiliation: Department of Thoracic Surgery, The Central Hospital, Baotou, Inner Mongolia, China.
authors.forename: Dong-Tao
authors.initials: DT
authors.lastname: Wang
authors.affiliation: Department of Endocrinology, Inner Mongolia North Heavy Industries Group Corp. Ltd Hospital (The Third Affiliated Hospital of Baotou Medical College), China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Yang
authors.affiliation: Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China. Electronic address: Pansuyue82@qq.com.
authors.forename: Su-Yue
authors.initials: SY
authors.lastname: Pan
keywords: HDAC-6; Lactacystin; PD cell model