首页> 外文期刊>Nature reviews neuroscience >Oroxylum indicum (L.) extract protects human neuroblastoma SH-SY5Y cells against beta-amyloid-induced cell injury
【24h】

Oroxylum indicum (L.) extract protects human neuroblastoma SH-SY5Y cells against beta-amyloid-induced cell injury

机译:炔烃铟(L.)提取物保护人神经母细胞瘤SH-SEN-SE5Y细胞免受β-淀粉样蛋白诱导的细胞损伤

获取原文
获取原文并翻译 | 示例
           

摘要

It has been reported that amyloid beta peptide, the major component of senile plaques, serves a critical role in the development and progression of Alzheimer's disease (AD) by generating reactive oxygen species (ROS), leading to oxidative stress. The aim of the present study was to investigate the protective effect of Oroxylum indicum (L.) extract against A beta 25-35-induced oxidative stress and cell injury using SH-SY5Y cells as a model, and at exploring the underlying mechanisms. The results revealed that the exposure of cells to 20 mu M A beta 25-35 significantly increased cellular oxidative stress, as evidenced by the increased ROS levels. A beta 25-35 treatment also increased caspase-3/7 activity and lactate dehydrogenase (LDH) release, and caused viability loss. Oroxylum indicum treatment not only attenuated the generation of ROS and suppressed caspase-3/7 activity but also reduced the neurotoxicity of A beta 25-35 in a concentration-dependent manner, as evidenced by the increased cell viability and decreased LDH release. Treatment with Oroxylum indicum also increased superoxide dismutase (SOD) and catalase (CAT) activity, increased the phosphorylation of Akt and cAMP-responsive element binding protein (CREB), and contributed to the upregulation of Bcl-2 protein. In combination, these results indicated that Oroxylum indicum extract could protect SH-SY5Y cells against A beta 25-35-induced cell injury, at least partly, by inhibiting oxidative stress, increasing SOD and CAT activity, attenuating caspase 3/7 activity and promoting the cell survival pathway, Akt/CREB/Bcl-2. The approach used in the present study may also be useful for preventing the neurotoxicity induced by A beta in AD and related neurodegenerative diseases. Further studies investigating the activity of Oroxylum indicum extract in vivo are now required.
机译:据报道,淀粉样蛋白β肽是老年斑块的主要成分,通过产生反应性氧物种(ROS)在阿尔茨海默病(AD)的开发和进展中发挥关键作用,导致氧化应激。本研究的目的是探讨奥诺斯税(L.)提取物对β25-35诱导的氧化应激和细胞损伤的保护作用,用SH-SY5Y细胞作为模型,探索潜在机制。结果表明,细胞暴露于20μm的β25-35显着增加了细胞氧化应激,如增加的ROS水平所证明。 β25-35处理也增加了Caspase-3/7活性和乳酸脱氢酶(LDH)释放,并引起了活力损失。奥罗生素贴花治疗不仅衰减了ROS和抑制的Caspase-3/7活性,而且还以浓度依赖性方式降低了β25-35的神经毒性,如提高的细胞活力和降低的LDH释放。用氧化锇抑制酶(SOD)和过氧化氢酶(CAT)活性的处理也增加了AKT和CAMP响应元件结合蛋白(CREB)的磷酸化,并有助于BCL-2蛋白的上调。组合,这些结果表明,通过抑制氧化应激,增加的SOD和猫活性,衰减Caspase 3/7活性和促进,葡萄醛蛋白蛋白蛋白提取物可以保护SH-SY5Y细胞免受β25-35诱导的细胞损伤诱导的细胞损伤。细胞存活途径,AKT / CREB ​​/ BCL-2。本研究中使用的方法也可用于预防AD和相关神经变性疾病中β的神经毒性。现在需要进一步研究研究体内体内钙氧化镁提取物的活性。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号