目的  研究帕金森病（PD）细胞模型中组蛋白去乙酰化酶6（HDAC6）的表达水平及其对α-突触核蛋白阳性包涵体的影响。方法  使用Lipofectamin 2000构建稳定过表达野生型α-突触核蛋白的人神经母细胞瘤SK-N-SH细胞，并加入蛋白酶体抑制剂lactacystin制作α-突触核蛋白异常聚集的PD模型；采用Western blotting检测HDAC6的表达水平；使用HDAC6特异性抑制剂tubacin处理后，免疫荧光染色检测α-突触核蛋白阳性的包涵体水平。结果  Lactacystin处理细胞的HDAC6表达水平较对照细胞明显升高，且α-突触核蛋白阳性的包涵体增多，而经tubacin处理后包涵体减少，差异均有统计学意义（P<0.05）。结论  在蛋白酶体抑制剂制作的PD细胞模型中，抑制升高的HDAC6可使α-突触核蛋白阳性的包涵体水平降低；其机制可能与HDAC6参与α-突触核蛋白从寡聚体向包涵体形式的转化从而起保护作用有关。

Objective  To investigate the expression of histone deacetylase 6 (HDAC6) and its effects on α-synuclein-positive inclusion bodies in the cell model of Parkinson's disease (PD). Methods  The human neuroblastoma cells SK-N-SH with stable over-expressed wild type α-synuclein were constructed via Lipofectamin 2000. The PD model with abnormal aggregation of α-synuclein was established by adding the proteasome inhibitor lactacystin. The expression of HDAC6 was detected by Western blotting. After being treated with HDAC6 specific inhibitor tubacin, the level of α-synuclein-positive inclusion bodies was detected by immunofluorescence staining. Results  Compared with the controls, the expression of HDAC6 of lactacystin-treated cells was significant higher and α-synuclein-positive inclusion bodies were more. Treatment by tubacin reduced the amount of inclusion bodies and the difference was statistically significant (P＜0.05). Conclusion  In the PD cell model established by proteasome inhibitor, inhibition of increased HDAC6 can reduce the amount of α-synuclein-positive inclusion bodies, which may be relevant to the involvement of HDAC6 in the conversion of α-synuclein from oligomers to inclusion bodies, so as to play a role of protection.