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CNS Neurosci Ther. 2012 Jan;18(1):14-20. doi: 10.1111/j.1755-5949.2011.00277.x.

A neuroprotective mechanism of YGY-E in cerebral ischemic injury in rats.

Author information

  • 1State Key Laboratory of New Drug & Pharmaceutical Process, Shanghai Institute of Pharmaceutical Industry, China.

Abstract

AIMS:

To investigate the anticerebral ischemic properties of YGY-E (apigenin-7-O-β-D-glucopyranosy l-4'-O-α-L-rhamnopy-ranosid, a flavonoid glycoside extracted from plant phoenix-tail fern), focusing on its effects on neuronal apoptosis.

METHODS:

In vitro YGY-E treatment was examined in primary cultured rat hippocampal neurons subjected to hypoxia-reoxygenation (H-R) injury. In addition, in vivo effects of YGY-E on neuronal apoptosis were measured by Hoechst staining and in situ DNA end labeling (TUNEL). Finally, B cell lymphoma/lewkmia-2 (Bcl-2) level in ischemic rat brain tissue was evaluated with immunohistochemistry and western blot analyses.

RESULTS:

In vitro YGY-E (50-100 μg/mL) treatment increased the survival rate compared to that of the vehicle-treated group (P < 0.05 and P < 0.01, respectively). In in vivo experiments, YGY-E (2.5-10 mg/kg) decreased the percentage of apoptotic neurons (P < 0.01), increased Bcl-2 (P < 0.01) in ischemic rat brain tissue. These effects were dose dependent.

CONCLUSIONS:

Our findings indicate that YGY-E's neuroprotective effects may be because of its inhibition of neuronal apoptosis by increasing Bcl-2 expression.

© 2012 Blackwell Publishing Ltd.

PMID:
22280158
[PubMed - indexed for MEDLINE]
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