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Inhibition of beta-amyloid-induced neurotoxicity by pinocembrin through Nrf2/HO-1 pathway in SH-SY5Y cells.
J Neurol Sci. 2016 Sep 15; 368:223-30.JN

Abstract

Amyloid beta peptide (Aβ) can cause neurotoxicity in Alzheimer's disease (AD). It evokes a cascade of oxidative damage to neurons. Pinocembrin (PCB), the most abundant flavonoid in propolis, has been proven to have neuroprotective effects in vivo and in vitro. In the present study, we investigated the neuroprotective effects of PCB on Aβ25-35-induced neurotoxicity. Exposure of SH-SY5Y cells to 25μM Aβ25-35 for 24h caused viability loss, apoptotic increase and reactive oxygen species (ROS) increase, pre-treatment with PCB for 4h significantly reduced the viability loss, apoptotic rate and attenuated Aβ-mediated ROS production. PCB strikingly inhibited Aβ25-35-induced mitochondrial dysfunctions, including lowered membrane potential, decreased Bcl-2/Bax ratio. In addition, PCB suppressed the release of cytochrome c and the cleavage of caspase-3. PCB treatment also resulted in an increase in Nrf2 protein levels and subsequent induction of heme oxygenase-1(HO-1) expression in SH-SY5Y cells. RNA interference-mediated knockdown of Nrf2 expression suppressed the PCB-induced HO-1 expression. Notably, we found that the HO-1 inhibitor zinc protoporphyrin IX (ZnPP) markedly diminished the neuroprotective effect of PCB against Aβ-mediated neurotoxicity. Taken together, these results indicated that PCB protects SH-SY5Y cells from Aβ25-35-induced neurotoxicity through activation of Nrf2/HO-1 pathways. Thus, activation of Nrf2/HO-1 pathways and inhibition of mitochondria-dependent apoptosis together may protect cells from Aβ25-35-induceded neurotoxicity.

Authors+Show Affiliations

Chifeng Medical College, Chifeng University, the Affiliated Hospital of Chifeng University, Chifeng 024005, PR China; Department of Oncology, the Affiliated Hospital of Chifeng University, Chifeng 024005, PR China.Department of Geriatrics, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, PR China.2012 MBBS, Chifeng Medical College, Chifeng University.Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100193, PR China.Chifeng Medical College, Chifeng University, the Affiliated Hospital of Chifeng University, Chifeng 024005, PR China.Department of Central Lab, the Affiliated Hospital of Chifeng University, Chifeng 024005, PR China.Department of Neurology, the Affiliated Hospital of Chifeng University, Chifeng 024005, PR China.Department of Neurology, the Affiliated Hospital of Chifeng University, Chifeng 024005, PR China.Chifeng Medical College, Chifeng University, the Affiliated Hospital of Chifeng University, Chifeng 024005, PR China; Department of Central Lab, the Affiliated Hospital of Chifeng University, Chifeng 024005, PR China; Department of Neurology, the Affiliated Hospital of Chifeng University, Chifeng 024005, PR China. Electronic address: whongquan@alu.fudan.edu.cn.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27538638

Citation

Wang, Yumin, et al. "Inhibition of Beta-amyloid-induced Neurotoxicity By Pinocembrin Through Nrf2/HO-1 Pathway in SH-SY5Y Cells." Journal of the Neurological Sciences, vol. 368, 2016, pp. 223-30.
Wang Y, Miao Y, Mir AZ, et al. Inhibition of beta-amyloid-induced neurotoxicity by pinocembrin through Nrf2/HO-1 pathway in SH-SY5Y cells. J Neurol Sci. 2016;368:223-30.
Wang, Y., Miao, Y., Mir, A. Z., Cheng, L., Wang, L., Zhao, L., Cui, Q., Zhao, W., & Wang, H. (2016). Inhibition of beta-amyloid-induced neurotoxicity by pinocembrin through Nrf2/HO-1 pathway in SH-SY5Y cells. Journal of the Neurological Sciences, 368, 223-30. https://doi.org/10.1016/j.jns.2016.07.010
Wang Y, et al. Inhibition of Beta-amyloid-induced Neurotoxicity By Pinocembrin Through Nrf2/HO-1 Pathway in SH-SY5Y Cells. J Neurol Sci. 2016 Sep 15;368:223-30. PubMed PMID: 27538638.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition of beta-amyloid-induced neurotoxicity by pinocembrin through Nrf2/HO-1 pathway in SH-SY5Y cells. AU - Wang,Yumin, AU - Miao,Yingchun, AU - Mir,Aamina Zia, AU - Cheng,Long, AU - Wang,Lina, AU - Zhao,Linan, AU - Cui,Qifu, AU - Zhao,Weili, AU - Wang,Hongquan, Y1 - 2016/07/11/ PY - 2016/04/11/received PY - 2016/07/03/revised PY - 2016/07/08/accepted PY - 2016/8/20/entrez PY - 2016/8/20/pubmed PY - 2017/5/20/medline KW - Alzheimer's disease KW - Beta amyloid KW - Heme oxygenase-1 KW - Neuroprotection KW - Nrf2 KW - Pinocembrin SP - 223 EP - 30 JF - Journal of the neurological sciences JO - J Neurol Sci VL - 368 N2 - Amyloid beta peptide (Aβ) can cause neurotoxicity in Alzheimer's disease (AD). It evokes a cascade of oxidative damage to neurons. Pinocembrin (PCB), the most abundant flavonoid in propolis, has been proven to have neuroprotective effects in vivo and in vitro. In the present study, we investigated the neuroprotective effects of PCB on Aβ25-35-induced neurotoxicity. Exposure of SH-SY5Y cells to 25μM Aβ25-35 for 24h caused viability loss, apoptotic increase and reactive oxygen species (ROS) increase, pre-treatment with PCB for 4h significantly reduced the viability loss, apoptotic rate and attenuated Aβ-mediated ROS production. PCB strikingly inhibited Aβ25-35-induced mitochondrial dysfunctions, including lowered membrane potential, decreased Bcl-2/Bax ratio. In addition, PCB suppressed the release of cytochrome c and the cleavage of caspase-3. PCB treatment also resulted in an increase in Nrf2 protein levels and subsequent induction of heme oxygenase-1(HO-1) expression in SH-SY5Y cells. RNA interference-mediated knockdown of Nrf2 expression suppressed the PCB-induced HO-1 expression. Notably, we found that the HO-1 inhibitor zinc protoporphyrin IX (ZnPP) markedly diminished the neuroprotective effect of PCB against Aβ-mediated neurotoxicity. Taken together, these results indicated that PCB protects SH-SY5Y cells from Aβ25-35-induced neurotoxicity through activation of Nrf2/HO-1 pathways. Thus, activation of Nrf2/HO-1 pathways and inhibition of mitochondria-dependent apoptosis together may protect cells from Aβ25-35-induceded neurotoxicity. SN - 1878-5883 UR - https://www.unboundmedicine.com/medline/citation/27538638/Inhibition_of_beta_amyloid_induced_neurotoxicity_by_pinocembrin_through_Nrf2/HO_1_pathway_in_SH_SY5Y_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-510X(16)30423-3 DB - PRIME DP - Unbound Medicine ER -