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MAPK 信号通路的激活会诱导冷应激青春期小鼠海马中促凋亡蛋白的上调。

Activation of the MAPK signaling pathway induces upregulation of pro-apoptotic proteins in the hippocampi of cold stressed adolescent mice.

机构信息

College of Animal Science and Veterinary Medicine, Heilongjiang Bayi Agricultural University, Daqing, 163319, PR China.

College of Food Science, Heilongjiang Bayi Agricultural University, Daqing, 163319, PR China.

出版信息

Neurosci Lett. 2019 Apr 23;699:97-102. doi: 10.1016/j.neulet.2018.12.028. Epub 2019 Jan 31.

Abstract

Stress induces many non-specific responses in the hippocampus, especially during adolescence. Low environmental temperature is known to induce stress, but its influence on the hippocampus, especially in adolescent mice is not clear. We compared apoptotic-related protein levels and MAPK signaling pathway activation in hippocampal neurons of adolescent mice under low temperature conditions (4 °C for 12 h) with western blotting and immunohistochemistry. Western bolt results demonstrated that the levels of phospho-JNK, phospho-p38, and cleaved-caspase 3 significantly increased, while the ratio of Bcl-XL/Bax decreased, in the cold stress group. The results of immunohistochemistry (IHC) and Nissl staining demonstrated that the protein optical density of caspase 3 increased and Nissl bodies decreased in the cold stress group compared with controls. Thus, we conclude that cold exposure initiates activation of the MAPK signaling pathway and subsequently induces the upregulation of pro-apoptotic proteins in the hippocampi of adolescent mice. Overall our study reveals the relationship between cold stress and apoptosis in adolescent mice.

摘要

应激在海马中诱导许多非特异性反应,尤其是在青春期。已知低温会引起应激,但它对海马的影响,特别是对青春期小鼠的影响尚不清楚。我们通过 Western blot 和免疫组织化学比较了低温条件(4°C 12 h)下青春期小鼠海马神经元中的凋亡相关蛋白水平和 MAPK 信号通路激活情况。Western blot 结果表明,冷应激组中磷酸化-JNK、磷酸化-p38 和 cleaved-caspase 3 的水平显著增加,而 Bcl-XL/Bax 的比值降低。免疫组织化学(IHC)和尼氏染色的结果表明,与对照组相比,冷应激组 caspase 3 的蛋白光密度增加,尼氏体减少。因此,我们得出结论,冷暴露会引发 MAPK 信号通路的激活,进而导致青春期小鼠海马中促凋亡蛋白的上调。总之,我们的研究揭示了冷应激与青春期小鼠凋亡之间的关系。

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