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首页> 外文期刊>Rejuvenation research >Phytohormone Abscisic Acid Protects Human Neuroblastoma SH-SY5Y Cells Against 6-Hydroxydopamine-Induced Neurotoxicity Through Its Antioxidant and Antiapoptotic Properties
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Phytohormone Abscisic Acid Protects Human Neuroblastoma SH-SY5Y Cells Against 6-Hydroxydopamine-Induced Neurotoxicity Through Its Antioxidant and Antiapoptotic Properties

机译:植物激素脱落酸通过其抗氧化剂和抗透露性能保护人类神经母细胞免受6-羟基多胺诱导的神经毒性

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摘要

Parkinson's disease (PD) is a destroying and prevalent neurodegenerative disease that is characterized by a progressive death of midbrain dopaminergic neurons. It is important to understand the possible neuroprotective effects of reagents that rescue the neurons from death and apoptosis. In this study, we investigated the effects of abscisic acid (ABA) on 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in human dopaminergic neuroblastoma SH-SY5Y cell line as an in vitro model of PD. Cell damage was induced by 150M 6-OHDA and the cell viability was examined by 2-[4,5-dimethyl-2-thiazolyl]-2,5-diphenyl-2-tetrazolium bromide (MTT) assay. Reactive oxygen species (ROS) and mitochondrial membrane potential were assessed by fluorescence probe methods. Biochemical markers of apoptosis were also determined by immunoblotting. The data showed that 6-OHDA caused a significant loss of cell viability and mitochondrial membrane potential. In addition, intracellular ROS, cleaved caspase-3, Bax:Bcl-2 ratio, and cytochrome c release were significantly increased in 6-OHDA-incubated cells. ABA (100M) elicited a significant protective effect and reduced biochemical markers of cell damage and death. Blockage of peroxisome proliferator-activated receptor (PPAR) completely prevented the effect of ABA on 6-OHDA-induced cell toxicity. The results suggest that ABA has neuroprotective property against 6-OHDA-induced neurotoxicity, which is performed through PPAR signaling. However, ABA antioxidant and antiapoptotic properties are involved, at least in part, in such protection.
机译:帕金森病(PD)是一种破坏和普遍的神经变性疾病,其特征是中脑多巴胺能神经元的渐进性。重要的是要了解从死亡和细胞凋亡中拯救神经元的可能神经保护作用。在这项研究中,我们研究了脱落酸(ABA)对6-羟基多胺(6-OHDA)的影响人的多巴胺能神经母细胞瘤SH-SY5Y细胞系中的神经毒性,作为PD的体外模型。将细胞损伤造成150m 6-OHDA,通过2- [4,5-二甲基-2-噻唑基] -2,5-二苯基-2-四唑溴(MTT)测定检查细胞活力。通过荧光探针方法评估反应性氧物质(ROS)和线粒体膜电位。通过免疫印迹也决定了细胞凋亡的生化标记。该数据显示6-OHDA导致细胞活力和线粒体膜电位显着丧失。另外,在6-OHDA - 孵育的细胞中,细胞内ROS,切割的Caspase-3,Bax:Bcl-2比和细胞色素C释放显着增加。 ABA(100米)引发了显着的保护作用,降低了细胞损伤和死亡的生化标志。过氧化物酶体增殖物激活受体(PPAR)的阻塞完全阻止了ABA对6- OHDA诱导的细胞毒性的影响。结果表明,ABA具有针对6- OHDA诱导的神经毒性的神经保护性,其通过PPAR信号传导进行。然而,至少部分地在这种保护中涉及ABA抗氧化剂和抗曝光性能。

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