Effects of rhIL-6 on Bcl-2 and Bax expression and apoptosis after anoxia-reoxygenation in cultured rat hippocampal neurons.
- Author:
Ai-Shi DING
1
;
Fu-Zhuang WANG
;
Li-Ying WU
;
Ming FAN
Author Information
1. Department of Neurobiology, Institute of Basic Medical Sciences, Academy of Military Medical Sciences, Beijing 100850.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
drug effects;
Cell Hypoxia;
drug effects;
physiology;
Cells, Cultured;
Hippocampus;
cytology;
Interleukin-6;
pharmacology;
Neurons;
drug effects;
physiology;
Proto-Oncogene Proteins;
biosynthesis;
Proto-Oncogene Proteins c-bcl-2;
biosynthesis;
Rats;
Rats, Wistar;
Recombinant Proteins;
pharmacology;
bcl-2-Associated X Protein
- From:
Acta Physiologica Sinica
2002;54(2):115-120
- CountryChina
- Language:Chinese
-
Abstract:
The purpose of the present study was to determine the effects of recombinant human interleukin-6 (rhIL-6) on the Bcl-2 and Bax expression and apoptosis after anoxia-reoxygenation in cultured rat hippocampal neurons. The control and rhIL-6 treated hippocampal neurons cultured for 12 d were exposed to anoxia environment (90% N2+10% CO2) for 2 and 4 h and then were reoxygenated for 24 and 72 h. The expression of Bcl-2 and Bax was revealed immunocytochemically using the antiserum against Bcl-2 and Bax. The apoptosis was examined by the terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nickel end labeling (TUNEL) method and flow cytometric analysis. The results showed that in cultured hippocampal neurons the Bcl-2 expression decreased while Bax expression and the percentage of apoptotic neurons increased after anoxia-reoxygenation compared with those before anoxia. In comparison with the control, after anoxia-reoxygenation the Bcl-2 expression in hippocampal neurons was higher than that in rhIL-6 group; however the Bax expression and the percentage of the apoptosis were decreased in rhIL-6 group. It is suggested that rhIL-6 may play a role in protecting neurons from the damage induced by anoxia-reoxygenation.
