Qin Xiao-Yan, Cheng Yong, Cui Jia, Zhang Yan, Yu Long-Chuan
Laboratory of Biotechnology and State Key Laboratory of Chinese Ethnic Minority Traditional Medicine, College of Life and Environmental Science, Minzu University of China, Beijing 100081, China.
Neurosci Lett. 2009 Oct 2;463(2):158-61. doi: 10.1016/j.neulet.2009.07.047. Epub 2009 Jul 22.
The present study explored the effect of curcumin against amyloid beta (Abeta)-induced toxicity on cultured rat primary prefrontal cortical neurons. The results showed that administration of 10 microM of curcumin induced significantly protection against 20 microM of Abeta(25-35)-induced toxicity on the cultured rat primary prefrontal cortical neurons tested by MTT and TUNEL assays. We further examined the involvements of the apoptotic or anti-apoptotic proteins in curcumin protection against Abeta(25-35)-induced cytotoxicity on cultured neurons and found that the content of apoptotic protein caspase-3 was increased and the content of anti-apoptotic factor Bcl2 was decreased significantly after Abeta(25-35) treatments, while administration of curcumin significantly inhibited the Abeta(25-35)-induced increases in the content of caspase-3 and inhibited the Abeta(25-35)-induced decreases in the content of Bcl2 tested by Western blot. The results suggest that curcumin protects cultured rat primary prefrontal cortical neurons against Abeta-induced cytotoxicity, and both Bcl2 and caspase-3 are involved in the curcumin-induced protective effects.
本研究探讨了姜黄素对培养的大鼠原代前额叶皮层神经元中β-淀粉样蛋白(Aβ)诱导的毒性的影响。结果表明,通过MTT和TUNEL检测,给予10微摩尔姜黄素可显著保护培养的大鼠原代前额叶皮层神经元免受20微摩尔Aβ(25-35)诱导的毒性。我们进一步研究了凋亡或抗凋亡蛋白在姜黄素保护培养神经元免受Aβ(25-35)诱导的细胞毒性中的作用,发现Aβ(25-35)处理后凋亡蛋白caspase-3的含量增加,抗凋亡因子Bcl2的含量显著降低,而通过蛋白质免疫印迹法检测发现,给予姜黄素可显著抑制Aβ(25-35)诱导的caspase-3含量增加,并抑制Aβ(25-35)诱导的Bcl2含量降低。结果表明,姜黄素可保护培养的大鼠原代前额叶皮层神经元免受Aβ诱导的细胞毒性,并且Bcl2和caspase-3均参与了姜黄素诱导的保护作用。