The Blood Component Iron Causes Neuronal Apoptosis Following Intracerebral Hemorrhage via the PERK Pathway.
The Blood Component Iron Causes Neuronal Apoptosis Following Intracerebral Hemorrhage via the PERK Pathway.
复制标题
血液成分铁通过 PERK 途径导致脑出血后神经元凋亡。
DOI：
10.3389/fneur.2020.588548
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发表时间：
2020
影响因子：
3.4
通讯作者：
Chen G
中科院分区：
文献类型：
--
作者：
Wu M;Gao R;Dang B;Chen G
PERK信号通路在脑出血后神经细胞凋亡中起重要作用。ICH可导致血液成分释放到大脑中。然而，血液中的哪种成分起主要作用仍不清楚。本研究旨在研究脑出血后不同血液成分中PERK通路的激活，并探讨哪些成分与神经细胞凋亡有主要关系。采用85只SD大鼠建立脑出血模型。免疫印迹（WB）和免疫荧光（IF）用于评估PERK通路的表达。采用TUNEL染色、FJC染色及神经功能评分评价脑出血后神经元凋亡和坏死情况。结果显示，脑出血后48 h，注射Fe 3+和Fe 2+可上调p-PERK和p-eIF 2 α蛋白水平。采用去铁胺（deferoxamine，DFX）法研究Fe ~（3+）通过PERK信号通路在脑出血中的作用。结果表明，注射DFX逆转了蛋白水平的增加，并阻止了神经元凋亡。因此，铁通过PERK信号通路在ICH中起重要作用。此外，铁的减少证明了ICH中的神经保护作用。这表明铁和PERK通路的靶向干预可能是改善ICH预后的有效治疗策略。
PERK signaling pathway plays an important role in neuronal apoptosis after Intracerebral hemorrhage (ICH). ICH can cause the release of blood components into the brain. However, which component in the blood plays a major role still unclear. This study was designed to investigate the activation of the PERK pathway in different blood components after ICH and explore which components have major relationships with neuronal apoptosis. Eighty-five Sprague–Dawley rats were used to establish an ICH model. Western blot (WB) and immunofluorescence (IF) were used to evaluate the expression of the PERK pathway. TUNEL staining, FJC staining and neurological score were used to evaluate neuronal apoptosis and necrosis after ICH. The results showed that protein levels of p-PERK and p-eIF2α were upregulated following ICH with the injection of Fe3+ and Fe2+ after 48 h. Then, deferoxamine (DFX) was used to study the roles of Fe3+ in ICH through the PERK signaling pathway. The results showed that injection of DFX reversed increasing protein levels and prevented neuronal apoptosis. Thus, iron plays an important role in ICH through the PERK signaling pathway. Furthermore, the reduction of iron demonstrates neuroprotective effects in ICH. This suggests that targeting intervention of the iron and PERK pathway could be an effective treatment strategy to improve ICH prognosis.
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