Effect of 2LMISEN® on Long-Term Hippocampal Neurons Culture as a Screening Senescent Cells Model: p16INK4A and Caspase 3 Quantification

N. L. Lilli, Delphine Révy, C. Volteau, S. Robelet, B. Lejeune
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引用次数: 2

Abstract

The aim of the present study was to investigate the effect of one capsule of the micro-immunotherapy medicine (MIM) 2LMISEN® compared to vehicle, in a neuronal aging model. Senescence and apoptosis of hippocampal neurons were evaluated by measuring p16INK4a and caspase 3 levels, respectively. The data presented is a single observation. Mice hippocampal neuron cultures were treated with MIM (11 mM) or vehicle (11 mM) from 22 days in vitro (DIV) until 27 DIV. After incubation, hippocampal neuron cultures were fixed at 15 (control condition), 22, 25 and 27 DIV and then incubated with primary antibodies p16INK4a, MAP2 and Caspase 3. Quantification of p16INK4a and Caspase 3-positive neurons was done using Developer software. We found that vehicle had no effect on p16INK4a expression, whereas MIM was able to decrease p16INK4a levels at 22, 25 and 27 DIV in a statistically significant manner. The MIM had no significative effect on Caspase 3 expression. Our preliminary results showed that the MIM capsule significantly reduced neuronal senescence and not apoptosis.
2LMISEN®作为筛选衰老细胞模型对海马神经元长期培养的影响:p16INK4A和Caspase 3定量
本研究的目的是在神经元衰老模型中,研究一粒微免疫疗法药物(MIM)2LMISEN®胶囊与载体相比的效果。通过分别测量p16INK4a和胱天蛋白酶3水平来评估海马神经元的衰老和凋亡。所提供的数据只是一个观察结果。从体外22天(DIV)到27天,用MIM(11mM)或载体(11mm)处理小鼠海马神经元培养基。孵育后,将海马神经元培养物固定在15(对照条件)、22、25和27 DIV,然后与一级抗体p16INK4a、MAP2和Caspase 3孵育。使用Developer软件对p16INK4a和Caspase 3阳性神经元进行定量。我们发现载体对p16INK4a的表达没有影响,而MIM能够以统计学显著的方式降低22、25和27 DIV时的p16INK4a水平。MIM对Caspase 3表达无明显影响。我们的初步结果表明,MIM胶囊显著降低了神经元衰老,而不是细胞凋亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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