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采用免疫组化方法，观察缺氧诱导体外培养大鼠海马神经元ｃ－ｆｏｓ的表达及人重组白细胞介素－１β（ｒｈＩＬ－１β）的影响。结果显示，缺氧后海马神经元中Ｆｏｓ染色阳性胞核的百分率随缺氧时间的延长而显著增加。图像分析的结果显示，缺氧后Ｆｏｓ染色阳性胞核的平均光密度亦随缺氧时间的延长而显著增加。经ｒｈＩＬ－１β孵育的神经元缺氧后Ｆｏｓ染色阳性胞核的百分率和Ｆｏｓ染色阳性胞核的平均光密度均明显低于对照组。本结果表明，缺氧能诱导体外培养海马神经元ｃ－ｆｏｓ表达，ｒｈＩＬ－１β能抑制缺氧神经元ｃ－ｆｏｓ表达。提示ｒｈＩＬ－１β对海马神经元缺氧损伤具有一定调控作用。
Immunohistochemistry was used to observe the expression of c-fos in hippocampal neurons induced by hypoxia and the effect of human recombinant interleukin-1β (rhIL-1β). The results showed that the percentage of positive Fos-stained nuclei in hippocampal neurons increased significantly after hypoxia. The results of image analysis showed that the average optical density of positive Fos-stained nuclei after hypoxia also increased significantly with the prolongation of hypoxia. The percentage of Fos-stained nuclei and the average optical density of Fos-stained nuclei in neurons incubated with rhIL-1β were significantly lower than those in control group. The results show that hypoxia can induce c-fos expression in cultured hippocampal neurons, rhIL-1β can inhibit c-fos expression in hypoxic neurons. These results suggest that rhIL-1β may play a regulatory role in hypoxic injury of hippocampal neurons.