Graduate Institute of Chinese Pharmaceutical Sciences, College of Pharmacy, China Medical University, Taichung, Taiwan, R.O.C.
Phytother Res. 2010 Jan;24 Suppl 1:S102-8. doi: 10.1002/ptr.2940.
The present study was carried out to investigate the neuroprotective effect of luteolin on amyloid beta (Abeta) (25-35)-induced neurotoxicity using cultured rat cortical neurons. After exposure of primary cultures of rat cortical cells to 10 muM Abeta (25-35) for 48 h, cortical cell cultures exhibited marked apoptotic death. Pretreatment with luteolin (1, 10 microM) significantly protected cortical cell cultures against Abeta (25-35)-induced toxicity. Luteolin (1, 10 microM) showed a concentration-dependent inhibition on 10 muM Abeta (25-35)-induced apoptotic neuronal death, as assessed by MTT assay. Furthermore, luteolin reduced apoptotic characteristics by DAPI staining. For Western blot analysis, the results showed that the protective effect of luteolin on Abeta (25-35)-induced neurotoxicity was mediated by preventing of ERK-p, JNK, JNK-p, P38-p and caspase 3 activations in rat primary cortical cultures. Taken together, the results suggest that luteolin prevents Abeta (25-35)-induced apoptotic neuronal death through inhibiting the protein level of JNK, ERK and p38 MAP kinases and caspase 3 activations.
本研究旨在探讨木樨草素对淀粉样β肽（Abeta）（25-35）诱导的神经毒性的神经保护作用，采用培养的大鼠皮质神经元进行研究。将大鼠皮质细胞原代培养物暴露于 10 μM Abeta（25-35）48 h 后，皮质细胞培养物表现出明显的凋亡性死亡。木樨草素（1、10 μM）预处理可显著保护皮质细胞培养物免受 Abeta（25-35）诱导的毒性。MTT 检测结果显示，木樨草素（1、10 μM）对 10 μM Abeta（25-35）诱导的凋亡性神经元死亡呈浓度依赖性抑制作用。此外，DAPI 染色显示木樨草素减少了凋亡特征。Western blot 分析结果表明，木樨草素对 Abeta（25-35）诱导的神经毒性的保护作用是通过阻止大鼠原代皮质培养物中 ERK-p、JNK、JNK-p、P38-p 和 caspase 3 的激活来介导的。综上所述，这些结果表明，木樨草素通过抑制 JNK、ERK 和 p38 MAP 激酶以及 caspase 3 的激活，防止 Abeta（25-35）诱导的凋亡性神经元死亡。
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