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The effect of selenium on the autophagy of macrophage infected by Staphylococcus aureus

机译:硒对金黄色葡萄球菌感染巨噬细胞自噬的影响

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摘要

Selenium can alleviate the inflammatory reaction infected by Staphylococcus aureus (S. aureus). However, the role of selenium on the autophagy in RAW264.7 macrophages infected by S. aureus has not been reported. The goal of this study was to clarify the effect of selenium on the autophagy and related inflammatory pathways (MAPK and NF-kappa B) in RAW264.7 macrophages infected by S. aureus. RAW264.7 macrophages were co-treated with Na2SeO3 and S. aureus. The expression of related inflammatory pathways (MAPK and NF-kappa B) and autophagy-related proteins were detected by Western blotting. The microtubule-binding protein light chain 3 (LC3) puncta were measured with immunofluorescence staining. The ultrastructure of RAW264.7 macrophages infected by S. aureus was detected by transmission electron microscope (TEM). And plate counting method was used to detect the proliferation of S. aureus in RAW264.7 macrophages. The results showed that the expression levels of LC3 II increased and the expression levels of p62 decreased after adding selenium, compared with S. aureus infection group. Compared with S. aureus infection group, the intracellular LC3 puncta and autophagic vesicles, autophagosomes, and autolysosomes increased with selenium supplementation. The number of S. aureus proliferation decreased with addition of selenium, compared with S. aureus infection group. Selenium could significantly inhibit the phosphorylation of MAPK and NF-kappa B signaling pathway key proteins, compared with S. aureus infection group. In summary, selenium could promote the autophagy in macrophages infected by S. aureus, alleviate the blockade of autophagic flow, depress the transcription of MAPK and NF-kappa B signaling pathways, and inhibit the proliferation of S. aureus in RAW264.7 macrophages.
机译:硒可以缓解葡萄球菌(金黄色葡萄球菌)感染的炎症反应。然而,尚未报告硒对粗糙的玉米金黄色葡萄球菌巨噬作用的作用。本研究的目的是阐明硒对由S.金黄色葡萄球菌感染的Raw264.7巨噬细胞的自噬和相关炎症途径(MAPK和NF-Kappa B)的影响。 Raw264.7巨噬细胞用Na2SeO3和金黄色葡萄球菌共同处理。通过蛋白质印迹检测相关炎症途径(MAPK和NF-Kappa B)和自噬相关蛋白的表达。用免疫荧光染色测量微管结合蛋白质轻链3(LC3)点。通过透射电子显微镜(TEM)检测由S.UUREUS感染的Raw264.7巨噬细胞的超微结构。和板数计数方法用于检测Raw264.7巨噬细胞中S. aureus的增殖。结果表明,与金黄色葡萄球菌感染组相比,加入硒后,LC3 II的表达水平和P62的表达水平降低。与S.UUREUS感染组相比,细胞内LC3点和自噬囊泡,自噬体和自糖,随着硒的补充而增加。与Aureus感染组相比,加入硒的S. aureus增殖的数量降低。与S.UUREUS感染组相比,硒可以显着抑制MAPK和NF-Kappa B信号通路键蛋白的磷酸化。总之,硒可以促进由S.UUREUS感染的巨噬细胞中的自噬,缓解自噬流动的阻断,压下MAPK和NF-Kappa B信中途径的转录,并抑制Raw264.7巨噬细胞中的S.UUREUS的增殖。

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