小胶质细胞
神经炎症
神经保护
巨噬细胞极化
炎症
吞噬作用
巨噬细胞
肿瘤坏死因子α
医学
免疫学
细胞生物学
生物
癌症研究
神经科学
化学
体外
生物化学
作者
Yang He,Yang Gao,Qiang Zhang,Guiyin Zhou,Fang Cao,Shengtao Yao
出处
期刊:Neuroscience
[Elsevier]
日期:2020-03-26
卷期号:437: 161-171
被引量:135
标识
DOI:10.1016/j.neuroscience.2020.03.008
摘要
Inflammatory damage following ICH is often attributed to microglia/macrophage activation. In many diseases, IL-4 has been proven to switch microglia/macrophages from the pro-inflammatory to the anti-inflammatory subtype. However, the role and underlying mechanism of IL-4 in ICH, especially in neuroprotection, remain unknown. In our study, we constructed a microglia/macrophage polarization model in BV2 cells to verify that the M2 shift of microglia/macrophages was mediated by JAK1/STAT6 after IL-4 treatment and then revealed that in vitro administration of IL-4 decreased M1 markers, pro-inflammatory cytokines and neuroapoptosis markers but significantly increased M2 markers and anti-inflammatory cytokines. Using an ICH model in mice, we observed that IL-4 administration decreased neurological deficits, brain edema and infarct lesions induced by ICH. We verified that IL-4 mediates inflammation by regulating M1/M2 polarization in ICH and explored the underlying mechanism. Furthermore, we discovered that pathway components and apoptosis-related proteins showed consistent trends based on their respective roles, and inferred that the process that TNF-α activates caspase-3 may be the crosstalk that microglia phagocytosis developed into accelerate apoptosis of cells in ICH. In conclusion, our study demonstrates that IL-4 may promote M2 microglia/macrophage polarization partly through the JAK1/STAT6 pathway to alleviate neuroinflammation after ICH.
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