文献类型：期刊文献

英文题名：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

作者：Zhang, Yi[1];Gong, Xiao-Gang[1,2];Sun, Hong-Mei[1];Guo, Zhen-Yu[1];Hu, Jing-Hong[3];Wang, Yuan-Yuan[1];Feng, Wan-Di[1];Li, Lin[4];Li, Ping[5];Wang, Zhen-Zhen[6];Chen, Nai-Hong[6,7]

第一作者：Zhang, Yi

通讯作者：Zhang, Y[1];Sun, HM[1]

机构：[1]Beijing Univ Chinese Med, Sch Tradit Chinese Med, Dept Anat, Beijing, Peoples R China;[2]Beijing Union Univ, Coll Special Educ, Beijing, Peoples R China;[3]Beijing Univ Chinese Med, Sch Tradit Chinese Med, Ctr Sci Res, Beijing, Peoples R China;[4]Capital Med Univ, Minist Educ, Key Lab Neurodegenerat Dis, Beijing, Peoples R China;[5]China Japan Friendship Hosp, Inst Clin Med Sci, Beijing Key Lab Immune Mediated Inflammatory Dis, Beijing, Peoples R China;[6]Chinese Acad Med Sci, Peking Union Med Coll, State Key Lab Bioact Subst & Funct Nat Med, Neurosci Ctr,Inst Mat Med, Beijing, Peoples R China;[7]Hunan Univ Chinese Med, Coll Pharm, Changsha, Hunan, Peoples R China

第一机构：Beijing Univ Chinese Med, Sch Tradit Chinese Med, Dept Anat, Beijing, Peoples R China

通讯机构：[1]corresponding author), Beijing Univ Chinese Med, Sch Tradit Chinese Med, Dept Anat, Beijing, Peoples R China.

年份：2018

卷号：9

期号：OCT

外文期刊名：FRONTIERS IN PHARMACOLOGY

收录：;Scopus(收录号：2-s2.0-85055148718);WOS:【SCI-EXPANDED(收录号:WOS:000447607000001)】；

基金：This study was supported by grants from the National Natural Science Foundation of China (Nos. 81473376, 81573773, and 81774110), Follow-Up Research Project of Beijing University of Chinese Medicine (No. 81202939), and Open Program of Key Laboratory of Neurodegenerative Diseases of Ministry of Education (Capital Medical University) (No. 2016SJBX03).

语种：英文

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

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.