[Anoxia-induced c-fos expression of cultured rat hippocampal neurons and effect of recombinant human interleukin-1 beta].
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.
D000818:Animals; D000831:Animals, Newborn; D015687:Cell Hypoxia; D002478:Cells, Cultured; D016762:Genes, fos; D006624:Hippocampus / Q000166:cytology*; D007375:Interleukin-1 / Q000494:pharmacology*; D053583:Interleukin-1beta; D009474:Neurons / Q000378:metabolism; D010446:Peptide Fragments / Q000494:pharmacology*; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis*; D051381:Rats; D017208:Rats, Wistar; D011994:Recombinant Proteins / Q000494:pharmacology