An Hong-Mei, Li Guo-Wen, Lin Chen, Gu Chao, Jin Miao, Sun Wen-Xian, Qiu Ming-Feng, Hu Bing
Pharmazie. 2014 May;69(5):391-5.
Amyloid-beta induced neurotoxicity has been identified as a major cause of Alzheimer's disease. Acorus tatarinowii Schott is one of the most frequently used Chinese herbs for Alzheimer's disease treatment. However, the effects of Acorus tatarinowii Schott on amyloid-beta mediated nerve cell damage remains unknown. In the present study, neuronal differentiated PC12 cells were used as a model to evaluate the effects of A. tatarinowii Schott extract (ATSE) against Abeta25-35 induced neurotoxicity. The results showed pretreatment with ATSE significantly protected PC12 cells from Abeta25-35 induced cell death, lactate dehydrogenase release, DNA damage, mitochondrial dysfunction and cytochrome c release from mitochondria. In addition, pretreatment with ATSE also significantly inhibited Abeta25-35 induced caspase-3 activation and reactive oxygen species generation in PC12 cells. These observations suggested that ATSE protects PC12 cells from amyloid-beta induced neurotoxicity.
β-淀粉样蛋白诱导的神经毒性已被确定为阿尔茨海默病的主要病因。石菖蒲是治疗阿尔茨海默病最常用的中草药之一。然而,石菖蒲对β-淀粉样蛋白介导的神经细胞损伤的影响尚不清楚。在本研究中,将神经元分化的PC12细胞作为模型,以评估石菖蒲提取物(ATSE)对β25-35诱导的神经毒性的影响。结果表明,用ATSE预处理可显著保护PC12细胞免受β25-35诱导的细胞死亡、乳酸脱氢酶释放、DNA损伤、线粒体功能障碍以及线粒体细胞色素c释放。此外,用ATSE预处理还可显著抑制β25-35诱导的PC12细胞中caspase-3活化和活性氧生成。这些观察结果表明,ATSE可保护PC12细胞免受β-淀粉样蛋白诱导的神经毒性。