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[重组人白细胞介素-6对培养的大鼠海马神经元缺氧复氧后Bcl-2和Bax表达及细胞凋亡的影响]

[Effects of rhIL-6 on Bcl-2 and Bax expression and apoptosis after anoxia-reoxygenation in cultured rat hippocampal neurons].

作者信息

Ding Ai-Shi, Wang Fu-Zhuang, Wu Li-Ying, Fan Ming

机构信息

Department of Neurobiology, Institute of Basic Medical Sciences, Academy of Military Medical Sciences, Beijing 100850.

出版信息

Sheng Li Xue Bao. 2002 Apr 25;54(2):115-20.

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.

摘要

本研究的目的是确定重组人白细胞介素-6(rhIL-6)对培养的大鼠海马神经元缺氧复氧后Bcl-2和Bax表达及细胞凋亡的影响。将培养12天的对照和rhIL-6处理的海马神经元暴露于缺氧环境(90% N2 + 10% CO2)中2小时和4小时,然后再复氧24小时和72小时。使用抗Bcl-2和Bax的抗血清通过免疫细胞化学方法检测Bcl-2和Bax的表达。通过末端脱氧核苷酸转移酶介导的生物素化脱氧尿苷三磷酸镍末端标记(TUNEL)法和流式细胞术分析检测细胞凋亡。结果显示,与缺氧前相比,培养的海马神经元在缺氧复氧后Bcl-2表达降低,而Bax表达和凋亡神经元百分比增加。与对照组相比,缺氧复氧后海马神经元中Bcl-2表达高于rhIL-6组;然而,rhIL-6组中Bax表达和凋亡百分比降低。提示rhIL-6可能在保护神经元免受缺氧复氧诱导的损伤中发挥作用。

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