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α-Arbutin Protects Against Parkinson’s Disease-Associated Mitochondrial Dysfunction In Vitro and In Vivo

  • Yaqi Ding
  • Deqin Kong
  • Tong Zhou
  • Nai-di Yang
  • Chenqi Xin
  • Jiajia Xu
  • Qi Wang
  • Hang Zhang
  • Qiong Wu
  • Xiaomei Lu
  • Kahleong Lim
  • Bo Ma
  • Chengwu ZhangEmail author
  • Lin LiEmail author
  • Wei Huang
Original Paper

Abstract

Parkinson’s disease (PD), the most common neurodegenerative movement disorder, is characterized by the progressive loss of dopaminergic neurons in substantia nigra. The underlying mechanisms of PD pathogenesis have not been fully illustrated and currently PD remains incurable. Accumulating evidences suggest that mitochondrial dysfunction plays pivotal role in the dopaminergic neuronal death. Therefore, discovery of novel and safe agent for rescuing mitochondrial dysfunction would benefit PD treatment. Here we demonstrated for the first time that α-Arbutin (Arb), a natural polyphenol extracted from Ericaceae species, displayed significant protective effect on the rotenone (Rot)-induced mitochondrial dysfunction and apoptosis of human neuroblastoma cell (SH-SY5Y). We further found that the neuroprotective effect of Arb was associated with ameliorating oxidative stress, stabilizing of mitochondrial membrane potential, and enhancing adenosine triphosphate production. To investigate the underlying mechanism, we checked the AMP-activated protein kinase and autophagy pathway and we found that both were involved in the neuroprotection of Arb. Moreover, we explored the protective effect of Arb in drosophila PD model and found that Arb rescued parkin deficiency-induced motor function disability and mitochondrial abnormality of drosophila. Taken together, our study demonstrated that Arb got excellent neuroprotective effect on PD models both in vitro and in vivo and Arb might serve as a potent therapeutic agent for the treatment of PD.

Keywords

α-Arbutin Parkinson’s disease Mitochondria Oxidative stress Autophagy 

Notes

Acknowledgements

This study was supported from the National Science Foundation of China (Grant Nos. 81672508, 81773802), and Jiangsu Provincial Foundation for Distinguished Young Scholars (BK20170041), Key University Science Research Project of Jiangsu Province (No. 16KJA180004), Natural Science Foundation of Shaanxi Province (2019JM-016), Fundamental Research Funds for the Central Universities and China-Sweden Joint Mobility Project (51811530018).

Compliance with Ethical Standards

Conflict of interests

The authors declare no conflict of interests.

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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  • Yaqi Ding
    • 1
  • Deqin Kong
    • 2
  • Tong Zhou
    • 1
  • Nai-di Yang
    • 1
  • Chenqi Xin
    • 1
  • Jiajia Xu
    • 1
  • Qi Wang
    • 1
  • Hang Zhang
    • 1
  • Qiong Wu
    • 1
  • Xiaomei Lu
    • 1
  • Kahleong Lim
    • 3
  • Bo Ma
    • 4
  • Chengwu Zhang
    • 1
    Email author
  • Lin Li
    • 1
    Email author
  • Wei Huang
    • 1
    • 5
  1. 1.Key Laboratory of Flexible Electronics (KLOFE) & Institute of Advanced Materials (IAM)Nanjing Tech University (NanjingTech)NanjingPeople’s Republic of China
  2. 2.Department of Toxicology, The Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, Shaanxi Provincial Key Lab of Free Radical Biology and Medicine, School of Public HealthThe Medical University of Air ForceXi’anPeople’s Republic of China
  3. 3.Department of Physiology, School of MedicineNational University of SingaporeSingaporeSingapore
  4. 4.School of Pharmaceutical SciencesNanjing Tech UniversityNanjingPeople’s Republic of China
  5. 5.Shaanxi Institute of Flexible Electronics (SIFE), Northwestern Polytechnical UniversityXi’anPeople’s Republic of China

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