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Protective effects of agmatine in rotenone-induced damage of human SH-SY5Y neuroblastoma cells: Fourier transform infrared spectroscopy analysis in a model of Parkinson's disease

机译:胍丁胺对鱼藤酮诱导的人SH-SY5Y神经母细胞瘤细胞的保护作用:帕金森病模型中的傅里叶变换红外光谱分析

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Agmatine is a novel neuromodulator that plays a protective role in the CNS in several models of cellular damage. However, the mechanisms involved in these protective effects in neurodegenerative diseases are poorly understood. Fourier transform infrared (FTIR) spectroscopy analysis detects biomolecular changes in disordered cells and tissues. In this report, we utilize FTIR spectroscopy to characteiize the changes in rotenone-induced damage in neuronal-like differentiated SH-SY5Y neuroblastoma cells in the presence or absence of agmatine. The analysis of the FTIR spectra demonstrates significant alterations in rotenone-treated cells, whereas the FTIR spectra obtained after pre-incubation with agmatine (250 nM) significantly reduces these redox alterations and more closely resembles those of the control cells. In particular, rotenone-damaged cells demonstrate spectral alterations related to amide I, which correspond to an increase in ;6-sheet components, and decreases in the amide II absorption intensity, suggesting a loss of N-H bending and C-N stretching. These alterations were also evident by Fourier self-deconvolution analysis. Thus, rotenone-induced increases in the levels of stretching vibration bandrelated to the protein carboxyl group would account for a significant amount of misfolded proteins in the cell. Agmatine effectively reduces these effects of rotenone on protein structure. In conclusion, antioxidant and scavenging properties of agmatine reduce rotenone-produced cellular damage at the level of protein structure. These, together with other previous observations, demonstrate the therapeutic potential of agmatine in the treatment of Parkinson's disease.
机译:胍丁胺是一种新型的神经调节剂,在多种细胞损伤模型中在中枢神经系统中起保护作用。然而,关于神经退行性疾病中这些保护作用的机制了解甚少。傅立叶变换红外(FTIR)光谱分析可检测出紊乱的细胞和组织中的生物分子变化。在此报告中,我们利用FTIR光谱表征了存在或不存在胍丁胺的情况下鱼藤酮诱导的神经元样分化的SH-SY5Y神经母细胞瘤细胞中鱼藤酮诱导的损伤的变化。 FTIR光谱分析表明鱼藤酮处理的细胞发生了显着变化,而与胍丁胺(250 nM)预温育后获得的FTIR光谱显着减少了这些氧化还原变化,并且与对照细胞更相似。特别是,鱼藤酮损坏的细胞表现出与酰胺I相关的光谱变化,这对应于; 6-sheet组分的增加,以及酰胺II吸收强度的降低,表明N-H弯曲和C-N拉伸损失。通过傅立叶自解卷积分析,这些变化也很明显。因此,鱼藤酮诱导的与蛋白质羧基有关的拉伸振动带水平的增加将解释细胞中大量错误折叠的蛋白质。胍丁胺有效降低鱼藤酮对蛋白质结构的这些影响。总之,胍丁胺的抗氧化剂和清除特性在蛋白质结构水平上减少了鱼藤酮产生的细胞损伤。这些以及其他先前的观察结果证明了胍丁胺在帕金森氏病治疗中的治疗潜力。

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