Neurochemical Research

, Volume 40, Issue 7, pp 1463–1471 | Cite as

Eriodictyol Attenuates β-Amyloid 25–35 Peptide-Induced Oxidative Cell Death in Primary Cultured Neurons by Activation of Nrf2

  • Xu Jing
  • Huanying Shi
  • Xiuying Zhu
  • Xinbing Wei
  • Manru Ren
  • Minxing Han
  • Dongmei Ren
  • Haiyan LouEmail author
Original Paper


Oxidative stress plays an important role in the pathogenesis of neurodegenerative diseases, including Alzheimer’s disease (AD). Eriodictyol, a flavonoid isolated from the Chinese herb Dracocephalum rupestre, has long been established as an antioxidant. The present study was designed to investigate the effect of eriodictyol on β-amyloid 25–35 peptide (Aβ25–35)-induced oxidative cell death in primary neurons and to explore the role of the nuclear factor erythroid-2-related factor 2/antioxidant response element (Nrf2/ARE) pathway in this process. For this purpose, primary cultures of cortical neurons were exposed to 15 μM Aβ25–35 in the absence or presence of eriodictyol (20, 40 and 80 μM). The results revealed that Aβ25–35-induced cytotoxicity and apoptotic characteristics such as activation of JNK/p38 apoptotic signaling pathway were effectively attenuated by eriodictyol pretreatment. Eriodictyol treatment also resulted in an increase in Nrf2 protein levels and subsequent activation of ARE pathway genes in primary cultured neurons. The protective effects of eriodictyol were attenuated by RNA interference-mediated knockdown of Nrf2 expression. Taken together, these results clearly demonstrate that eriodictyol protects neurons against Aβ25–35-induced cell death partially through Nrf2/ARE signaling pathway, which further supports that eriodictyol might be a promising novel therapeutic agent for AD.


Alzheimer’s disease Eriodictyol Nrf2 Oxidative stress β-Amyloid 



This study was supported by Grants from the National Natural Science Foundation of China (Nos. 81274124 and 81173528) and Shandong Province Science and Technology Program (No. 2014GSF118038).

Conflict of interest

The authors declare that there are no conflicts of interest.


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Copyright information

© Springer Science+Business Media New York 2015

Authors and Affiliations

  • Xu Jing
    • 1
    • 4
  • Huanying Shi
    • 1
  • Xiuying Zhu
    • 2
  • Xinbing Wei
    • 1
  • Manru Ren
    • 1
  • Minxing Han
    • 1
  • Dongmei Ren
    • 3
  • Haiyan Lou
    • 1
    Email author
  1. 1.Department of Pharmacology, School of MedicineShandong UniversityJinanChina
  2. 2.Department of NeurosurgeryYucheng Renmin HospitalYuchengChina
  3. 3.Department of Natural Product Chemistry, Key Lab of Chemical Biology of MOE (Ministry of Education)Shandong UniversityJinanChina
  4. 4.Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of MedicineShandong UniversityJinanChina

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