Open AccessA Neuroprotective Mechanism of YGY‐E in Cerebral Ischemic Injury in Rats
Author(s) -
An YongTong,
Zhu Peng,
Zhong Yan,
Sheng YuChen,
Zhao Zhen,
Min Yang,
Xia YuYe
Publication year - 2012
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/j.1755-5949.2011.00277.x
Subject(s) - neuroprotection , apoptosis , tunel assay , in vivo , apigenin , pharmacology , western blot , ischemia , hypoxia (environmental) , chemistry , biology , medicine , flavonoid , biochemistry , microbiology and biotechnology , organic chemistry , oxygen , gene , antioxidant
SUMMARY 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.