胍丁胺抑制缺氧诱导的视网膜神经节细胞tnf - α释放。

Samin Hong, Kyoungsoo Park, C. Kim, G. Seong
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引用次数: 24

摘要

研究了缺氧对转化大鼠视网膜神经节细胞(RGCs)肿瘤坏死因子- α (tnf - α)释放的影响以及胍丁氨酸对缺氧诱导的RGCs肿瘤坏死因子- α生成的影响。RGCs在5%氧气的低氧条件下培养,加或不加100 μ m胍。Western blot检测tnf - α及其受体1 (TNF-R1)的表达水平。缺氧6小时后,我们注意到RGCs中tnf - α的产生增加。Agmatine在缺氧治疗12小时后显著降低tnf - α水平。TNF-R1的表达不受缺氧和agmatine处理的影响。我们的研究结果表明,agmatine在缺氧条件下抑制RGCs的tnf - α产生。这些结果表明,agmatine可能具有抗RGCs缺氧损伤的神经保护机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Agmatine inhibits hypoxia-induced TNF-alpha release from cultured retinal ganglion cells.
The effect of hypoxia on the release of tumor necrosis factor-alpha (TNF-alpha) in transformed rat retinal ganglion cells (RGCs) and the effect of agmatine on the hypoxia-induced production of TNF-alpha in RGCs were evaluated. RGCs were cultured under hypoxic conditions with 5% oxygen, with or without 100 microM agmatine. The expression levels of TNF-alpha and its receptor-1 (TNF-R1) were investigated by Western blot analysis. After 6 hours of hypoxia, we noted an increase in TNF-alpha production in RGCs. Agmatine significantly reduced TNF-alpha level after 12 hours of hypoxic treatment. The expression of TNF-R1 was not affected by the hypoxia or agmatine treatment. Our results show that agmatine inhibits the TNF-alpha production of RGCs in hypoxic condition. These results demonstrate a possible neuroprotective mechanism for agmatine against hypoxic damage in RGCs.
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