首页> 外文期刊>Neuroimmunomodulation >Inhalation of low-level formaldehyde increases the Bcl-2/Bax expression ratio in the hippocampus of immunologically sensitized mice.
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Inhalation of low-level formaldehyde increases the Bcl-2/Bax expression ratio in the hippocampus of immunologically sensitized mice.

机译:吸入低水平的甲醛会增加免疫敏化小鼠海马中的Bcl-2 / Bax表达比。

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OBJECTIVE: A recent study from our research group showed that repeated exposure to low-level formaldehyde (FA) increases the production of nerve growth factor, involving the survival and maintenance of neurons, in the hippocampus of immunized mice. In the present study, we examined the effects of FA on apoptotic mechanisms regulating survival and death of cells and on N-methyl-D-aspartate (NMDA) receptors related to hippocampal functions in the mouse hippocampus. METHODS: Western blot analyses were performed for Bcl-2, Bax and NMDA receptor subtypes 2A and 2B of the hippocampus taken from C3H mice exposed to 0 or 400 ppb of FA with or without ovalbumin (OVA) immunization. Immunohistochemical analysis for active caspase-3 was also carried out for these mice. RESULTS: The ratio of Bcl-2 to Bax expression levels significantly increased with 400-ppb FA exposure in OVA-immunized mice but not in mice without OVA immunization, although differences in each protein level were not significant among groups. Active caspase- 3-immunoreactive cells were found in the hippocampus. However, the number was only a few and not significantly affected by FA exposure and OVA immunization. NMDA receptor type 2A and 2B expression levels of FA-exposed mice were sustained at comparative levels with those for the control mice with or without OVA immunization. CONCLUSIONS: These results indicate that changes in the Bcl-2/Bax expression ratio, which occurs with low-level FA exposure and immunization and may follow enhancement of nerve growth factor production, exerts a protective effect against cell death by apoptosis.
机译:目的:我们研究小组的最新研究表明,反复接触低水平甲醛(FA)可增加免疫小鼠海马中神经生长因子的产生,涉及神经元的存活和维持。在本研究中,我们研究了FA对调节细胞存活和死亡的凋亡机制以及与小鼠海马海马功能相关的N-甲基-D-天冬氨酸(NMDA)受体的影响。方法:对暴露于0或400 ppb FA或无卵白蛋白(OVA)免疫的C3H小鼠的海马Bcl-2,Bax和NMDA受体亚型2A和2B进行Western印迹分析。还对这些小鼠进行了活性caspase-3的免疫组织化学分析。结果:OVA免疫小鼠中,暴露于400 ppb FA时,Bcl-2与Bax表达水平的比率显着增加,但未进行OVA免疫的小鼠中Bcl-2与Bax表达水平的比率却明显增加,尽管各组蛋白水平的差异并不显着。在海马中发现了活跃的caspase-3免疫反应性细胞。然而,该数目仅为少数并且不受FA暴露和OVA免疫的显着影响。暴露于FA的小鼠的NMDA受体2A和2B型表达水平与具有或不具有OVA免疫的对照小鼠的水平保持相对水平。结论:这些结果表明Bcl-2 / Bax表达比的变化,发生在低水平的FA暴露和免疫中,并且可能跟随神经生长因子产生的增强,对细胞凋亡的细胞死亡具有保护作用。

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