氧化应激
炎症
巨噬细胞极化
化学
精氨酸酶
基础(医学)
表型
细胞生物学
巨噬细胞
内分泌学
内科学
生物
分子生物学
免疫学
生物化学
医学
体外
氨基酸
精氨酸
基因
胰岛素
作者
Robert A. Yokel,Marsha L. Ensor,Hemendra J. Vekaria,Patrick G. Sullivan,David J. Feola,Arnold J. Stromberg,Michael T. Tseng,Douglas A. Harrison
标识
DOI:10.1016/j.nano.2022.102565
摘要
It was hypothesized that the catalyst nanoceria can increase inflammation/oxidative stress from the basal and reduce it from the elevated state. Macrophages clear nanoceria. To test the hypothesis, M0 (non-polarized), M1- (classically activated, pro-inflammatory), and M2-like (alternatively activated, regulatory phenotype) RAW 264.7 macrophages were nanoceria exposed. Inflammatory responses were quantified by IL-1β level, arginase activity, and RT-qPCR and metabolic changes and oxidative stress by the mito and glycolysis stress tests (MST and GST). Morphology was determined by light microscopy, macrophage phenotype marker expression, and a novel three-dimensional immunohistochemical method. Nanoceria blocked IL-1β and arginase effects, increased M0 cell OCR and GST toward the M2 phenotype and altered multiple M1- and M2-like cell endpoints toward the M0 level. M1-like cells had greater volume and less circularity/roundness. M2-like cells had greater volume than M0 macrophages. The results are overall consistent with the hypothesis.
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