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Nrf-2/HO-1 激活可防止金属焊接烟尘 UFPs 引起的 16HBE 细胞氧化应激和炎症。

Nrf-2/HO-1 activation protects against oxidative stress and inflammation induced by metal welding fume UFPs in 16HBE cells.

机构信息

Shanghai Municipal Center for Disease Control & Prevention, Shanghai, 200336, China.

State Environmental Protection Key Laboratory of Environmental Health Impact Assessment of Emerging Contaminants, Shanghai, 200233, China.

出版信息

Sci Rep. 2024 Oct 14;14(1):24057. doi: 10.1038/s41598-024-74599-8.

DOI:10.1038/s41598-024-74599-8
PMID:39402078
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11473639/
Abstract

As one of the main occupational hazards, welding fumes can cause oxidative damage and induce series of diseases, such as COPD or asthma. To clarify the effects of the metal fume ultrafine particulates (MF-UFPs) of welding fumes on oxidative damage, UFPs were collected by melt inert gas (MIG) and manual metal arc (MMA) welding, and the composition was confirmed. Human bronchial epithelial 16HBE cells were treated with 0-1000 µg/cm MF-UFPs to analyse the cytotoxicity, oxidative stress and cytokines. The protein and mRNA expression of Keap1-Nrf-2/antioxidant response elements (AREs) signalling pathway components were also analysed. After 4 h of treatment, the cell viability decreased 25% after 33.85 and 32.81 µg/cm MIG/MMA-UFPs treated. The intracellular ATP concentrations were also decreased significantly, while LDH leakage was increased. The decreased mitochondrial membrane potential and increased ROS suggested the occurrence of oxidative damage, and the results of proteome profiling arrays also showed a significant increase in IL-6 and IL-8. The expression of AREs which related to antioxidant and anti-inflammatory were also increased. These results indicate that the MF-UFPs can cause oxidative stress in 16HBE cells and activate the Nrf-2/ARE signalling pathway to against oxidative damage.

摘要

作为主要的职业危害之一，焊接烟雾会导致氧化损伤，并引起一系列疾病，如 COPD 或哮喘。为了阐明焊接烟雾金属烟炱超细颗粒（MF-UFPs）对氧化损伤的影响，采用惰性气体保护金属极电弧（MIG）和手工金属电弧（MMA）焊接收集 UFPs，并确定其成分。用人支气管上皮 16HBE 细胞用 0-1000μg/cm MF-UFPs 处理，分析细胞毒性、氧化应激和细胞因子。还分析了 Keap1-Nrf-2/抗氧化反应元件（AREs）信号通路成分的蛋白质和 mRNA 表达。处理 4 小时后，33.85 和 32.81μg/cm MIG/MMA-UFPs 处理后细胞活力分别下降 25%。细胞内 ATP 浓度也显著降低，而 LDH 漏出增加。线粒体膜电位降低和 ROS 增加表明发生了氧化损伤，蛋白质组谱分析阵列的结果也显示 IL-6 和 IL-8 显著增加。与抗氧化和抗炎相关的 AREs 的表达也增加。这些结果表明，MF-UFPs 可引起 16HBE 细胞氧化应激，并激活 Nrf-2/ARE 信号通路以对抗氧化损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e1c/11473639/d83bec019e32/41598_2024_74599_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e1c/11473639/50120c61e491/41598_2024_74599_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e1c/11473639/887aeeb83717/41598_2024_74599_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e1c/11473639/bde2a09c57a1/41598_2024_74599_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e1c/11473639/845553856ea5/41598_2024_74599_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e1c/11473639/d83bec019e32/41598_2024_74599_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e1c/11473639/50120c61e491/41598_2024_74599_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e1c/11473639/887aeeb83717/41598_2024_74599_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e1c/11473639/bde2a09c57a1/41598_2024_74599_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e1c/11473639/845553856ea5/41598_2024_74599_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e1c/11473639/d83bec019e32/41598_2024_74599_Fig6_HTML.jpg

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