Ezaki Yasuyuki, Nishihara Eijun, Shibata Yoshisada, Matsuo Takayuki, Kitagawa Naoki, Nagata Izumi, Shinohara Kazuyuki
Division of Neurobiology and Behavior, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Neuroreport. 2005 Aug 1;16(11):1163-7. doi: 10.1097/00001756-200508010-00006.
The accumulation of damage caused by oxidative stress exacerbates cell death in many neurodegenerative diseases. We evaluated the mechanism of neuronal cell death raised by glutamate-induced toxicity, using the immortalized mouse hippocampal cell line HT-22. Our results showed that vitamin E prevented glutamate-induced cell death, accompanied by the decline of cyclooxygenase-2 expression confirmed by reverse transcriptase polymerase chain reaction and immunocytochemistry. Moreover, the neuroprotection was still effective even when vitamin E was supplied after glutamate treatment. The decline of cyclooxygenase-2 activity was also highly correlated with the neural protective effect against glutamate-induced toxicity. These results represent new insights about the timing of vitamin E supplementation after toxic stimulation and one mechanism by which vitamin E could prevent neuronal cell death by controlling cyclooxygenase-2 activity.
氧化应激造成的损伤积累会加剧许多神经退行性疾病中的细胞死亡。我们使用永生化小鼠海马细胞系HT-22评估了谷氨酸诱导的毒性引发神经元细胞死亡的机制。我们的结果表明，维生素E可预防谷氨酸诱导的细胞死亡，同时逆转录聚合酶链反应和免疫细胞化学证实环氧合酶-2表达下降。此外，即使在谷氨酸处理后提供维生素E，神经保护作用仍然有效。环氧合酶-2活性的下降也与针对谷氨酸诱导毒性的神经保护作用高度相关。这些结果代表了关于毒性刺激后补充维生素E时机的新见解，以及维生素E通过控制环氧合酶-2活性预防神经元细胞死亡的一种机制。
