摘要
目的探讨牵正散合大补阴丸(QZS&DBYW)对1-甲基-4-苯基吡啶(MPP+)诱导的帕金森病(PD)细胞模型线粒体的影响,为深入探讨中药防治PD提供实验依据。方法选择人多巴胺能神经母细胞瘤SH-SY5Y,用MPP+处理建立PD细胞模型,采用QZS&DBYW干预。CCK-8法检测各组细胞存活率,Mito TrackerRed CMXRos(MTR)对活细胞线粒体标记,共聚焦显微镜观察,Image J软件测量线粒体形态因子和长宽比。结果 MPP+处理后细胞存活率有明显下降,QZS&DBYW干预不会明显改变细胞存活率。相较于空白对照组,模型组细胞出现大量空泡,线粒体长宽比显著降低,线粒体碎片明显增多。单独施用低浓度QZS&DBYW后线粒体分支增加,而高浓度中药使线粒体更为短小。低浓度QZS&DBYW治疗组可增加PD细胞的线粒体长度。结论牵正散和大补阴丸两方合用可减少线粒体的碎裂,在一定程度上对PD细胞模型线粒体有一定保护作用。
Objective To study the impacts of qianzheng san plus dabuyin wan（ QZS ＆ BDYW）on mitochondria in Parkinson＇s disease（PD） cell model induced by MPP^＋ so as to deeply explore the prevention and treatment of PD with Chinese medicine and provide the experimental evidence. Methods SH - SYSY was selected and MPP ＋ treatment was adopted to set up PD cell model. QZS ＆ BDYW was applied for intervention. CCK -8 method was used to detect the cell survival rate in each group. Mito Tracker Red CMXRos （MTR） was adopted to label mitochondria of living cell. The eonfocal microscopy was used for observation. JmageJ software was used to measure morphologie factor and the ratio of length and width of mitochondria. Results After MPP^ ＋ treatment, the cell survival rate was reduced apparently. The intervention of QZS ＆ BDYW did not obviously change the cell survival rate. Corresponding to the blank control group, a large amount of vacuoles appeared in cell of the model group, the length and width ratio of mitochondria was reduced significantly and mitochondria fragments were increased apparently. The mitochondria branches were increased after the use of QZS ＆ BDYW at low concentration and mitoehondria became much smaller after the use of Chinese medicine at high concentration. In the treatment group, QZS ＆ BDYW at low concentration increased mitochondria length in PD cell. Conclusion Qianzheng san and dabuyin wan in combination reduce mitoehondria fragmentation and bring a certain protective role for mitoehondria in PD cell model.
出处
《世界中西医结合杂志》
2015年第4期487-492,共6页
World Journal of Integrated Traditional and Western Medicine
基金
帕金森病研究北京市重点实验室开放课题项目(2013PJSB04)
