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PLoS One. 2012;7(5):e37540. doi: 10.1371/journal.pone.0037540. Epub 2012 May 22.

Soy isoflavones genistein and daidzein exert anti-apoptotic actions via a selective ER-mediated mechanism in neurons following HIV-1 Tat(1-86) exposure.

Author information

1
Department of Psychology, University of South Carolina, Columbia, South Carolina, United States of America. Adamssm4@mailbox.sc.edu

Abstract

BACKGROUND:

HIV-1 viral protein Tat partially mediates the neural dysfunction and neuronal cell death associated with HIV-1 induced neurodegeneration and neurocognitive disorders. Soy isoflavones provide protection against various neurotoxic insults to maintain neuronal function and thus help preserve neurocognitive capacity.

METHODOLOGY/PRINCIPAL FINDINGS:

We demonstrate in primary cortical cell cultures that 17β-estradiol or isoflavones (genistein or daidzein) attenuate Tat(1-86)-induced expression of apoptotic proteins and subsequent cell death. Exposure of cultured neurons to the estrogen receptor antagonist ICI 182,780 abolished the anti-apoptotic actions of isoflavones. Use of ERα or ERβ specific antagonists determined the involvement of both ER isoforms in genistein and daidzein inhibition of caspase activity; ERβ selectively mediated downregulation of mitochondrial pro-apoptotic protein Bax. The findings suggest soy isoflavones effectively diminished HIV-1 Tat-induced apoptotic signaling.

CONCLUSIONS/SIGNIFICANCE:

Collectively, our results suggest that soy isoflavones represent an adjunctive therapeutic option with combination anti-retroviral therapy (cART) to preserve neuronal functioning and sustain neurocognitive abilities of HIV-1 infected persons.

PMID:
22629415
PMCID:
PMC3358258
DOI:
10.1371/journal.pone.0037540
[Indexed for MEDLINE]
Free PMC Article
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