A Neuroprotective Mechanism of YGY-E in Cerebral Ischemic Injury in Rats


Yang Min and Yu-Ye Xia, Department of Pharmacology, Shanghai Institute of Pharmaceutical Industry, 1111 North Zhong Shan No1 Road, Shanghai 200437, China. Tel.: +86-21-55514600; Fax: +86-21-65449361; E-mail: Chenguoze@gmail.com and xiayuye2004@126.com Received 2 September 2011; revision 28 September 2011; accepted 2 October 2011


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.