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Articles, Neurobiology of Disease

BDNF Mediates Neuroprotection against Oxygen-Glucose Deprivation by the Cardiac Glycoside Oleandrin

Michael J. Van Kanegan, Dong Ning He, Denise E. Dunn, Peiying Yang, Robert A. Newman, Anne E. West and Donald C. Lo
Journal of Neuroscience 15 January 2014, 34 (3) 963-968; DOI: https://doi.org/10.1523/JNEUROSCI.2700-13.2014
Michael J. Van Kanegan
1Center for Drug Discovery and
2Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27704, and
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Dong Ning He
1Center for Drug Discovery and
2Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27704, and
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Denise E. Dunn
1Center for Drug Discovery and
2Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27704, and
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Peiying Yang
3Department of Experimental Therapeutics, The University of Texas, M. D. Anderson Cancer Center, Houston, Texas 77030
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Robert A. Newman
3Department of Experimental Therapeutics, The University of Texas, M. D. Anderson Cancer Center, Houston, Texas 77030
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Anne E. West
2Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27704, and
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Donald C. Lo
1Center for Drug Discovery and
2Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27704, and
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Abstract

We have previously shown that the botanical drug candidate PBI-05204, a supercritical CO2 extract of Nerium oleander, provides neuroprotection in both in vitro and in vivo brain slice-based models for focal ischemia (Dunn et al., 2011). Intriguingly, plasma levels of the neurotrophin BDNF were increased in patients treated with PBI-05204 in a phase I clinical trial (Bidyasar et al., 2009). We thus tested the hypothesis that neuroprotection provided by PBI-05204 to rat brain slices damaged by oxygen-glucose deprivation (OGD) is mediated by BDNF. We found, in fact, that exogenous BDNF protein itself is sufficient to protect brain slices against OGD, whereas downstream activation of TrkB receptors for BDNF is necessary for neuroprotection provided by PBI-05204, using three independent methods. Finally, we provide evidence that oleandrin, the principal cardiac glycoside component of PBI-05204, can quantitatively account for regulation of BDNF at both the protein and transcriptional levels. Together, these findings support further investigation of cardiac glycosides in providing neuroprotection in the context of ischemic stroke.

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The Journal of Neuroscience: 34 (3)
Journal of Neuroscience
Vol. 34, Issue 3
15 Jan 2014
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BDNF Mediates Neuroprotection against Oxygen-Glucose Deprivation by the Cardiac Glycoside Oleandrin
Michael J. Van Kanegan, Dong Ning He, Denise E. Dunn, Peiying Yang, Robert A. Newman, Anne E. West, Donald C. Lo
Journal of Neuroscience 15 January 2014, 34 (3) 963-968; DOI: 10.1523/JNEUROSCI.2700-13.2014

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BDNF Mediates Neuroprotection against Oxygen-Glucose Deprivation by the Cardiac Glycoside Oleandrin
Michael J. Van Kanegan, Dong Ning He, Denise E. Dunn, Peiying Yang, Robert A. Newman, Anne E. West, Donald C. Lo
Journal of Neuroscience 15 January 2014, 34 (3) 963-968; DOI: 10.1523/JNEUROSCI.2700-13.2014
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