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抗炎细胞因子 TGF-β1 和 IL-10 发挥抗缺氧作用并消除海马脑片神经元的缺氧后过度兴奋:比较方面。

Anti-inflammatory cytokines, TGF-β1 and IL-10, exert anti-hypoxic action and abolish posthypoxic hyperexcitability in hippocampal slice neurons: comparative aspects.

机构信息

Institute of Theoretical and Experimental Biophysics of Russian Academy of Sciences, Pushchino, Moscow Region, 142290, Russia.

出版信息

Exp Neurol. 2011 Dec;232(2):329-32. doi: 10.1016/j.expneurol.2011.09.004. Epub 2011 Sep 16.

Abstract

The aim of this study was to investigate the comparative effects of transforming growth factor β1 (TGF-β1) and interleukin-10 (IL-10) on the repeated brief hypoxia-induced alterations in the activity of hippocampal slice CA1 pyramidal neurons. The method of field potentials measurement in CA1 region of hippocampal slices was used. The principal results of our work are summarized as follow. 1. TGF-β1 reduces the depressive effect of brief hypoxia on the population spike amplitude more effectively than IL-10. 2. During TGF-β1 exposure (in contrast to IL-10), three 3-min hypoxic episodes do not induce the rapid hypoxic preconditioning. 3. TGF-β1 and IL-10 equally abolish posthypoxic hyperexcitability induced by repeated brief episodes of hypoxia in CA1 pyramidal neurons. These findings indicated that TGF-β1 and IL-10 are able to evoke anti-hypoxic effect and abolish the development of posthypoxic hyperexcitability induced by repeated brief hypoxic episodes in hippocampal CA1 pyramidal neurons. Our results also demonstrated that TGF-β1 reduced the effectiveness of hypoxia to depress neuronal activity more effectively than IL-10. We suggest that the present findings allow to explain the certain neuroprotective mechanisms of IL-10 and TGF-beta1 in the early phase of hypoxia and indicate that a therapeutic anti-inflammatory approach using these substances can provide neuroprotection in the brain hypoxic conditions.

摘要

本研究旨在探讨转化生长因子β1(TGF-β1)和白细胞介素 10(IL-10)对反复短暂缺氧诱导海马切片 CA1 锥体神经元活性改变的比较作用。采用海马切片 CA1 区场电位测量方法。我们工作的主要结果总结如下。1. TGF-β1 比 IL-10 更有效地减轻短暂缺氧对群体锋电位幅度的抑制作用。2. 在 TGF-β1 暴露期间(与 IL-10 相反),三个 3 分钟的缺氧期不会引起快速缺氧预处理。3. TGF-β1 和 IL-10 同样消除了反复短暂缺氧引起的 CA1 锥体神经元的缺氧后过度兴奋。这些发现表明,TGF-β1 和 IL-10 能够引发抗缺氧作用,并消除反复短暂缺氧引起的海马 CA1 锥体神经元的缺氧后过度兴奋的发展。我们的结果还表明,TGF-β1 比 IL-10 更有效地降低了缺氧抑制神经元活动的效果。我们认为,目前的发现可以解释 IL-10 和 TGF-β1 在缺氧早期的某些神经保护机制,并表明使用这些物质进行治疗性抗炎方法可以在脑缺氧条件下提供神经保护。

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