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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 3507290, 10 pages
Research Article

Inhibition of HSP90 Promotes Neural Stem Cell Survival from Oxidative Stress through Attenuating NF-κB/p65 Activation

1Department of Neurology, Jinling Hospital, Medical School of Nanjing University, 305 East Zhongshan Road, Nanjing, Jiangsu 210002, China
2School of Dentistry, Cardiff Institute of Tissue Engineering and Repair, Cardiff University, Heath Park, Cardiff CF14 4XY, UK
3State Key Laboratory of Military Stomatology & National Clinical Research Centre for Oral Diseases & Shaanxi Key Laboratory of Oral Diseases, Department of Operative Dentistry & Endodontics, School of Stomatology, Fourth Military Medical University, No. 145 Western Changle Road, Xi’an, Shaanxi 710032, China
4Department of Chemistry & Chemical Biology, MSC03 2060, University of New Mexico, Clark Hall B58, Albuquerque, NM 87131-0001, USA
5College of Chemistry and Materials Science, Jiangsu Key Laboratory of Biofunctional Materials, Nanjing Normal University, Nanjing 210023, China

Received 8 June 2016; Revised 23 August 2016; Accepted 25 August 2016

Academic Editor: Javier Egea

Copyright © 2016 Qian Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Stem cell survival after transplantation determines the efficiency of stem cell treatment, which develops as a novel potential therapy for several central nervous system (CNS) diseases in recent decades. The engrafted stem cells face the damage of oxidative stress, inflammation, and immune response at the lesion point in host. Among the damaging pathologies, oxidative stress directs stem cells to apoptosis and even death through several signalling pathways and DNA damage. However, the in-detail mechanism of stem cell survival from oxidative stress has not been revealed clearly. Here, in this study, we used hydrogen peroxide (H2O2) to induce the oxidative damage on neural stem cells (NSCs). The damage was in consequence demonstrated involving the activation of heat shock protein 90 (HSP90) and NF-B/p65 signalling pathways. Further application of the pharmacological inhibitors, respectively, targeting at each signalling indicated an upper-stream role of HSP90 upon NF-B/p65 on NSCs survival. Preinhibition of HSP90 with the specific inhibitor displayed a significant protection on NSCs against oxidative stress. In conclusion, inhibition of HSP90 would attenuate NF-B/p65 activation by oxidative induction and promote NSCs survival from oxidative damage. The HSP90/NF-B mechanism provides a new evidence on rescuing NSCs from oxidative stress and also promotes the stem cell application on CNS pathologies.