Da-Bu-Yin-Wan Improves the Ameliorative Effect of DJ-1 on Mitochondrial Dysfunction Through Augmenting the Akt Phosphorylation in a Cellular Model of Parkinson’s Disease

Frontiers in Pharmacology

Ping Li¹  Jing-Hong Hu²  Nai-Hong Chen³  Xiao-Gang Gong⁴  Hong-Mei Sun⁵  Zhen-Yu Guo⁵  Yuan-Yuan Wang⁵  Wan-Di Feng⁵  Yi Zhang⁵  Lin Li⁶  Zhen-Zhen Wang⁷ 

[1] Beijing Key Lab for Immune-Mediated Inflammatory Diseases, Institute of Clinical Medical Science, China-Japan Friendship Hospital, Beijing, China;Center for Scientific Research, School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China;College of Pharmacy, Hunan University of Chinese Medicine, Changsha, China;College of Special Education, Beijing Union University, Beijing, China;Department of Anatomy, School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China;Key Laboratory for Neurodegenerative Diseases of Ministry of Education, Capital Medical University, Beijing, China;State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Neuroscience Center, Institute of Materia Medica, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China;

关键词: Da-Bu-Yin-Wan;    Parkinson’s disease;    DJ-1;    Akt;    mitochondrial function;   

DOI  :  10.3389/fphar.2018.01206

来源: DOAJ

【 摘 要 】

Da-Bu-Yin-Wan (DBYW) is recorded originally in China over six centuries ago, and it is used to treat Parkinson’s disease (PD) clinically in recent decades. DJ-1 is a homodimeric protein linked to early-onset PD, and found in the mitochondria. In addition, DJ-1 could protect the cells by regulating gene transcription and modulating the Akt signal pathways. Therefore, in this research, we aimed to investigate the ameliorative effect of DBYW on mitochondria in the view of the DJ-1 and Akt signaling. Rat adrenal pheochromocytoma cell line PC-12 was transfected with the plasmid pcDNA3-Flag-DJ-1 (pDJ-1). Subsequently, PC-12 cells were exposed to the PD-related mitochondrial toxin (1-methyl-4-phenylpyridinium) without/with the DBYW. After transfected with the plasmid pDJ-1, the 1-methyl-4-phenylpyridinium-induced toxicity was decreased, and the DJ-1 expression in protein level was increased. DJ-1 overexpression not only increased the mitochondrial mass, but also improved the total ATP content. Moreover, Akt phosphorylation was augmented by DJ-1 overexpression. Additionally, DBYW enhanced the above effects. Conclusively, these findings indicate that DBYW promotes the ameliorative effects of DJ-1 on mitochondrial dysfunction at least through augmenting the Akt phosphorylation in 1-methyl-4-phenylpyridinium-treated PC-12 cells.

【 授权许可】

Unknown