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[缺氧诱导培养大鼠海马神经元c-fos表达及重组人白细胞介素-1β的作用]

[Anoxia-induced c-fos expression of cultured rat hippocampal neurons and effect of recombinant human interleukin-1 beta].

作者信息

Ding A, Wang F, Liu Z, Wan Q, Ling S

机构信息

Institute of Basic Medical Sciences, Academy of Military Medical Sciences, Beijing.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 1997 Nov;13(4):290-301.

Abstract

Effects of recombinant human interleukin-1 beta (rhIL-1 beta) on the c-fos expression of cultured rat hippocampal neurons in vitro induced by anoxia were studied by using an immunohistochemical method. The results showed that the percentage and the mean optical density of the Fos-positive neuronal nuclei in cultured hippocampal neurons increased markedly as anoxia prolonged, while those in hippocampal neurons pretreated with rhIL-1 beta were significantly lower than those of control. The results indicate that anoxia can induce c-fos expression of cultured rat hippocampal neurons in vitro and this can be inhibited by rhIL-1 beta, suggesting that rhIL-1 beta may protect neurons from damage in a certain degree during anoxia.

摘要

采用免疫组织化学方法研究重组人白细胞介素-1β(rhIL-1β)对体外培养的大鼠海马神经元缺氧诱导的c-fos表达的影响。结果显示,随着缺氧时间延长,培养的海马神经元中Fos阳性神经元细胞核的百分比和平均光密度显著增加,而预先用rhIL-1β处理的海马神经元中的百分比和平均光密度明显低于对照组。结果表明,缺氧可诱导体外培养的大鼠海马神经元的c-fos表达,而rhIL-1β可抑制这种表达,提示rhIL-1β在缺氧期间可能在一定程度上保护神经元免受损伤。

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