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首页> 外文期刊>Molecular Neurobiology >Inhibition of the Receptor for Advanced Glycation End-Products (RAGE) Attenuates Neuroinflammation While Sensitizing Cortical Neurons Towards Death in Experimental Subarachnoid Hemorrhage
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Inhibition of the Receptor for Advanced Glycation End-Products (RAGE) Attenuates Neuroinflammation While Sensitizing Cortical Neurons Towards Death in Experimental Subarachnoid Hemorrhage

机译：抑制对先进的糖糖末端产物（RAGE）的受体衰减神经炎症，同时敏感皮质神经元的实验性蛛网膜下腔中的死亡

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摘要

Subarachnoid hemorrhage (SAH) is a threatening and devastating neurological insult with high mortality and morbidity rates. Despite considerable efforts, the underlying pathophysiological mechanisms are still poorly understood. The receptor for advanced glycation end products (RAGE) is a multiligand receptor that has been implicated in various pathological conditions. We previously showed that RAGE was upregulated and may be involved in pathophysiology of SAH. In the current study, we investigated its potential role in SAH. We found that the upregulation of RAGE after SAH was NF-kappa B-dependent positive feedback regulation. Further, pharmacological inhibition of RAGE attenuated neuroinflammation, indicating a possible contributive role of RAGE in inflammation-associated brain injury after SAH. Conversely, however, inhibition of RAGE sensitized neurons, exacerbating cell death, which correlated with augmented apoptosis and diminished autophagy, suggesting that activation of RAGE may protect against SAH-induced neuronal injury. Furthermore, we demonstrate that inhibition of RAGE significantly reduced brain edema and improved neurological function at day 1 but not at day 3 post-SAH. Taken together, these results suggest that RAGE exerts dual role after SAH. Our findings also suggest caution should be exercised in setting RAGE-targeted treatment for SAH.
机译：蛛网膜下腔出血（SAH）是一种威胁性和毁灭性的神经系统侮辱，具有高死亡率和发病率。尽管努力相当努力，但潜在的病理生理机制仍然很清楚。先进的糖化末端产物（RAGE）的受体是一种多硅受体，其涉及各种病理条件。我们以前表明愤怒是上调的并且可能参与SAH的病理生理学。在目前的研究中，我们调查了其在SAH中的潜在作用。我们发现SAH后愤怒的上调是NF-KAPPA B依赖性阳性反馈调节。此外，药理抑制RAGE衰减神经炎性炎症，表明愤怒在SAH后炎症相关脑损伤中的可能作用作用。然而，相反，抑制愤怒致敏神经元，加剧细胞死亡，与增强的凋亡和自噬减少相关，表明愤怒的激活可以防止Sah诱导的神经元损伤。此外，我们证明患有危害的抑制显着降低了脑水肿，并在第1天改善了神经功能，但第3天后3天。总之，这些结果表明，愤怒在SAH后发挥了双重作用。我们的调查结果还建议谨慎在为SAH制定愤怒目标待遇时行使。

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