State Key Laboratory of New Drug & Pharmaceutical Process, Shanghai Institute of Pharmaceutical Industry, China.
CNS Neurosci Ther. 2012 Jan;18(1):14-20. doi: 10.1111/j.1755-5949.2011.00277.x.
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.
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.
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.
Our findings indicate that YGY-E's neuroprotective effects may be because of its inhibition of neuronal apoptosis by increasing Bcl-2 expression.
研究从植物海金沙中提取的黄酮苷元芹菜素-7-O-β-D-吡喃葡萄糖基-4'-O-α-L-鼠李吡喃糖苷（YGY-E）的抗脑缺血作用，重点探讨其对神经元凋亡的影响。
在体外培养的原代大鼠海马神经元缺氧再复氧（H-R）损伤模型中观察 YGY-E 的作用。此外，通过 Hoechst 染色和原位末端标记（TUNEL）检测 YGY-E 对体内神经元凋亡的影响。最后，通过免疫组化和 Western blot 分析评估缺血性大鼠脑组织中 B 细胞淋巴瘤/白血病-2（Bcl-2）的水平。
体外 YGY-E（50-100μg/ml）处理组与对照组相比，细胞存活率明显提高（P<0.05 和 P<0.01）。在体内实验中，YGY-E（2.5-10mg/kg）剂量依赖性地降低了凋亡神经元的比例（P<0.01），增加了缺血性大鼠脑组织中的 Bcl-2（P<0.01）。
我们的研究结果表明，YGY-E 的神经保护作用可能是通过增加 Bcl-2 的表达抑制神经元凋亡。
