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空气污染颗粒物诱导 RAW 264.7 巨噬细胞基因表达变化:内毒素的作用。

Gene Expression Changes Induced by Exposure of RAW 264.7 Macrophages to Particulate Matter of Air Pollution: The Role of Endotoxins.

机构信息

Department of Brain Biochemistry, Maj Institute of Pharmacology, Polish Academy of Sciences, 31-343 Kraków, Poland.

Department of Molecular Neuropharmacology, Maj Institute of Pharmacology, Polish Academy of Sciences, 31-343 Kraków, Poland.

出版信息

Biomolecules. 2022 Aug 10;12(8):1100. doi: 10.3390/biom12081100.

DOI:10.3390/biom12081100
PMID:36008994
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9405577/
Abstract

Despite the variable chemical and physical characteristics of particulate air pollutants, inflammation and oxidative stress have been identified as common mechanisms for cell damage and negative health influences. These effects are produced by organic components, especially by endotoxins. This study analyzed the gene expression profile after exposure of RAW 264.7 cells to the standard particulate matter (PM) material, NIST1648a, and PM with a reduced organic matter content, LAp120, in comparison to the effects of lipopolysaccharide (LPS). The selected parameters of cell viability, cell cycle progression, and metabolic and inflammatory activity were also investigated. Both forms of PM negatively influenced the parameters of cell activity. These results were generally reflected in the gene expression profile. Only NIST1648a, excluding LAp120, contained endotoxins and showed small but statistically significant pro-inflammatory activity. However, the gene expression profiling revealed strong pro-inflammatory cell activation induced by NIST1648a that was close to the effects of LPS. Changes in gene expression triggered by LAp120 were relatively small. The observed differences in the effects of NIST1648a and LAp120 were related to the content of organic matter in which bacterial endotoxins play an important role. However, other organic compounds and their interactions with other PM components also appear to be of significant importance.

摘要

尽管颗粒物空气污染物具有不同的化学和物理特性,但炎症和氧化应激已被确定为细胞损伤和负面健康影响的共同机制。这些作用是由有机成分产生的,特别是内毒素。本研究分析了 RAW 264.7 细胞暴露于标准颗粒物(PM)物质 NIST1648a 和有机物质含量降低的 PM(LAp120)后,与脂多糖(LPS)的作用相比,基因表达谱。还研究了细胞活力、细胞周期进程以及代谢和炎症活性的选定参数。两种形式的 PM 都对细胞活性参数产生负面影响。这些结果通常反映在基因表达谱中。只有 NIST1648a(不包括 LAp120)含有内毒素,并表现出微小但具有统计学意义的促炎活性。然而,基因表达谱分析显示,NIST1648a 诱导的强烈促炎细胞激活接近于 LPS 的作用。LAp120 引发的基因表达变化相对较小。观察到的 NIST1648a 和 LAp120 作用的差异与有机物含量有关,其中细菌内毒素起着重要作用。然而,其他有机化合物及其与其他 PM 成分的相互作用似乎也非常重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/4f06849635de/biomolecules-12-01100-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/442d1aadf5b4/biomolecules-12-01100-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/444880d4762b/biomolecules-12-01100-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/4ad482783888/biomolecules-12-01100-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/aa2ca715e931/biomolecules-12-01100-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/9b18b0b1d28a/biomolecules-12-01100-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/e317d013bc74/biomolecules-12-01100-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/d37fc8b3a46d/biomolecules-12-01100-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/2dacf8ee7fb3/biomolecules-12-01100-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/4f06849635de/biomolecules-12-01100-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/442d1aadf5b4/biomolecules-12-01100-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/444880d4762b/biomolecules-12-01100-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/4ad482783888/biomolecules-12-01100-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/aa2ca715e931/biomolecules-12-01100-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/9b18b0b1d28a/biomolecules-12-01100-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/e317d013bc74/biomolecules-12-01100-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/d37fc8b3a46d/biomolecules-12-01100-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/2dacf8ee7fb3/biomolecules-12-01100-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d55/9405577/4f06849635de/biomolecules-12-01100-g009.jpg

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