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  • Meeting abstract
  • Open Access

Curcumin protects SH-SY5Y cells from oxidative stress by up-regulating HO-1 via Phosphatidylinositol 3 Kinase/Akt/Nrf-2 and down-regulating HO-2

Contributed equally
Molecular Neurodegeneration20127 (Suppl 1) :S14

  • Published:


  • Curcumin
  • Ferritin
  • Polyphenol
  • Central Nervous System Disease
  • Nervous System Disease


Oxidative stress is considered to have a causative role in the development of central nervous system diseases, such as Alzheimer’s disease, Parkinson’s disease, tumor, etc. Curcumin, a polyphenol extracted from rhizomes of the plant Curcuma longa, is widely reported to have diverse anti-oxidative stress effects, but the underlying mechanism has not been fully elucidated. We investigated the mechanism underlying the neuroprotective properties of curcumin in human neuroblastoma SH-SY5Y cells subjected to oxidative stress.


The cells were treated with curcumin at different concentration (0, 1.25, 5, 20 μM) for 24, 48, 72 h, and/or with PI3K inhibitor LY294002 or Nrf-2 siRNA, the concentration- and time-dependent protection of curcumin against H2O2-induced toxicity was measured as ROS production and reduced cell growth. RT-PCR and Western blot were applied for detecting the expression of HO-1, HO-2, PI3K, AKT and Nrf-2 at mRNA and protein levels, also, the production of ferritin was measured by WB.


The expression of HO-1 and the production of ferritin were significantly increased, but the expression of HO-2 was decreased. Furthermore, curcumin could significantly induce the protein and mRNA expression of PI3K, AKT and Nrf-2 (P<0.05), while the protective effects of curcumin were prevented by PI3K inhibitor LY294002 or Nrf-2 siRNA.


Taken together, the data show that the cytoprotection of curcumin against oxidative stress in SH-SY5Y cells is by up-regulating HO-1 expression via PI3K/AKT/Nrf-2 intracellular signaling pathway and down-regulating HO-2 expression. Which suggests that curcumin is beneficial in the prevention and treatment of some CNS disease.


Authors’ Affiliations

Department of Pathology, Chongqing, Chongqing Medical University, 400016, China
Chongqing Key Laboratory of Neurobiology, Chongqing Medical University, Chongqing, 400016, China
Institute of Neuroscience, Chongqing Medical University, Yuzhong District Yuanjiagang Yixueyuan Road No.1, Chongqing, 400016, China


© Yin et al; licensee BioMed Central Ltd. 2012

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.