Liu Cuifang, Huang Xiaobo, Qiu Shengxiang, Chen Wenqiang, Li Weihong, Zhang Haiyan, Wang Tao, Wang Xue, Wu Xiling
Department of Chinese Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China.
Key Laboratory of Plant Resources Conservation and Sustainable Utilization, Guangdong Provincial Key Laboratory of Applied Botany, South China Botanical Garden, Chinese Academy of Sciences, Guangzhou, China.
Evid Based Complement Alternat Med. 2019 Mar 13;2019:8920813. doi: 10.1155/2019/8920813. eCollection 2019.
Autophagy plays an important role in the development of Parkinson disease (PD). Previous studies showed that autophagy could protect cells from -synuclein toxicity and promote functional coupling of mitochondria. But it is still a question whether modulating autophagy can be used to treat PD. In traditional Chinese medicine, a specific Chinese herbal complex called Bu Shen Jie Du Fang (BSJDF) has a long history of treating motor impairments similar to Parkinson disease, while its mechanism is still unclear. As a pilot study, we aimed to evaluate the efficacy and its mechanism of Bu Shen Jie Du Fang in an MPP-induced cell model of Parkinson's disease. And the phase contrast microscope (PCM) revealed that the BSJDF group had the greatest surviving cell counts compared with all other treated cell groups except the normal group. And Cell Counting Kit 8 (CCK8) assays showed a similar result. In BSJDF group, 3.7 ×10 cells/dish was identified by hemocytometer counts, which was significantly higher than other groups except the normal cells (p<0.05). In the BSJDF group, autophagy can be observed by transmission electron microscopy (TEM). Protein expression of Atg12 and LC3 in the BSJDF group was upregulated compared to the PD model group (p<0.05). Atg12 mRNA expression was also upregulated in the BSJDF group (p<0.05). In conclusion, our study indicated that the therapeutic mechanisms of BSJDF may be mediated by stimulating autophagy, and modulating autophagy can be used to treat PD.
自噬在帕金森病(PD)的发展过程中发挥着重要作用。先前的研究表明,自噬可以保护细胞免受α-突触核蛋白毒性的影响,并促进线粒体的功能耦合。但调节自噬是否可用于治疗PD仍是一个问题。在传统中医中,一种名为补肾解毒方(BSJDF)的特定中草药复方治疗类似于帕金森病的运动障碍已有很长历史,但其机制仍不清楚。作为一项初步研究,我们旨在评估补肾解毒方在MPP诱导的帕金森病细胞模型中的疗效及其机制。相差显微镜(PCM)显示,与除正常组之外的所有其他处理细胞组相比,BSJDF组存活细胞计数最多。细胞计数试剂盒8(CCK8)检测显示了类似结果。在BSJDF组中,通过血细胞计数器计数确定为3.7×10个细胞/培养皿,这明显高于除正常细胞之外的其他组(p<0.05)。在BSJDF组中,可通过透射电子显微镜(TEM)观察到自噬现象。与PD模型组相比,BSJDF组中Atg12和LC3的蛋白表达上调(p<0.05)。BSJDF组中Atg12 mRNA表达也上调(p<0.05)。总之,我们的研究表明,补肾解毒方的治疗机制可能是通过刺激自噬介导的,调节自噬可用于治疗PD。