Cong Lin, Cao Chang, Cheng Yong, Qin Xiao-Yan
Beijing Engineering Research Center of Food Environment and Health, Minzu University of China, Beijing 100081, China; Department of General Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
Beijing Engineering Research Center of Food Environment and Health, Minzu University of China, Beijing 100081, China; College of Life & Environmental Science, Minzu University of China, Beijing 100081, China.
Oxid Med Cell Longev. 2016;2016:2050435. doi: 10.1155/2016/2050435. Epub 2015 Dec 15.
Green tea polyphenols are a natural product which has antioxidative and antiapoptotic effects. It has been shown that glutamate excitotoxicity induced oxidative stress is linked to neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. In this study we explored the neuroprotective effect of green teen polyphenols against glutamate excitotoxicity in the primary cultured cortical neurons. We found that green tea polyphenols protected against glutamate induced neurotoxicity in the cortical neurons as measured by MTT and TUNEL assays. Green tea polyphenols were then showed to inhibit the glutamate induced ROS release and SOD activity reduction in the neurons. Furthermore, our results demonstrated that green tea polyphenols restored the dysfunction of mitochondrial pro- or antiapoptotic proteins Bax, Bcl-2, and caspase-3 caused by glutamate. Interestingly, the neuroprotective effect of green tea polyphenols was abrogated when the neurons were incubated with siBcl-2. Taken together, these results demonstrated that green tea polyphenols protected against glutamate excitotoxicity through antioxidative and antiapoptotic pathways.
绿茶多酚是一种具有抗氧化和抗凋亡作用的天然产物。研究表明，谷氨酸兴奋性毒性诱导的氧化应激与阿尔茨海默病和帕金森病等神经退行性疾病有关。在本研究中，我们探讨了绿茶多酚对原代培养皮层神经元中谷氨酸兴奋性毒性的神经保护作用。我们发现，通过MTT和TUNEL检测，绿茶多酚可保护皮层神经元免受谷氨酸诱导的神经毒性。随后发现绿茶多酚可抑制神经元中谷氨酸诱导的ROS释放和SOD活性降低。此外，我们的结果表明，绿茶多酚可恢复由谷氨酸引起的线粒体促凋亡或抗凋亡蛋白Bax、Bcl-2和caspase-3的功能障碍。有趣的是，当神经元与siBcl-2一起孵育时，绿茶多酚的神经保护作用被消除。综上所述，这些结果表明绿茶多酚通过抗氧化和抗凋亡途径保护神经元免受谷氨酸兴奋性毒性的损伤。
