Journal
JOURNAL OF THE NEUROLOGICAL SCIENCES
Volume 368, Issue -, Pages 223-230Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jns.2016.07.010
Keywords
Pinocembrin; Beta amyloid; Nrf2; Heme oxygenase-1; Neuroprotection; Alzheimer's disease
Categories
Funding
- National Natural Science Foundation of China [81450036, 81260196]
- Program for Young Talents of Science and Technology in Universities of Inner Mongolia Autonomous Region (IMAR) [NJYT-13-B20]
- Natural Science Foundation of IMAR [2014MS0892, 2014BS0802, 2014MS0814, 2015BS0812, 2013MS1176]
- National Social Science Foundation of China [13CRK009]
- Scientific Research Projects in Universities of IMAR [NJZY234, NJZZ14271]
- Program for Young Innovative Talents of IMAR
- Talent development fund of IMAR
- Program for Grasslands Talents of IMAR
- Program of IMAR Key Laboratory of Human Genetics
- New Century 321 Talents Project of IMAR
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Amyloid beta peptide (A beta) 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 A beta(25-35)-induced neurotoxicity. Exposure of SH-SY5Y cells to 25 mu M A beta(25-35) for 24 h caused viability loss, apoptotic increase and reactive oxygen species (ROS) increase, pre-treatment with PCB for 4 h significantly reduced the viability loss, apoptotic rate and attenuated A beta-mediated ROS production. PCB strikingly inhibited A beta(25-35)-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 A beta-mediated neurotoxicity. Taken together, these results indicated that PCB protects SH-SY5Y cells from A beta(25-35)-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 A(25-35)-induceded neurotoxicity. (C) 2016 Elsevier B.V. All rights reserved.
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