上海大学学报(自然科学版) ›› 2024, Vol. 30 ›› Issue (2): 218-228.doi: 10.12066/j.issn.1007-2861.2551

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老化黑碳颗粒诱导人神经母细胞瘤细胞SH-SY5Y 炎症反应及机制

黄津, 王田田, 安静, 钟玉芳, 尚羽   

  1. 上海大学 环境与化学工程学院 环境污染与健康研究所, 上海 200444
  • 出版日期:2024-04-30 发布日期:2024-05-14
  • 通讯作者: 尚 羽 (1982—), 女, 副研究员, 博士, 研究方向为大气污染与人体健康. E-mail:yushang@shu.edu.cn
  • 基金资助:
    国家自然科学面上基金资助项目 (41977366)

Oxidized black carbon induced inflammatory responses and associated mechanisms in SH-SY5Y cells

HUANG Jin, WANG Tiantian, AN Jing, ZHONG Yufang, SHANG Yu   

  1. Institute of Environmental Pollution and Health, School of Environmental and Chemical Engineering, Shanghai University, Shanghai 200444, China
  • Online:2024-04-30 Published:2024-05-14

摘要: 以人神经母细胞瘤细胞 SH-SY5Y 为研究对象, 分析被臭氧氧化的黑碳 (oxidized black carbon, OBC) 颗粒引起的炎症反应以及核因子-κB (nuclear factor-κB, NF-κB) 和磷脂酰肌醇3 激酶(phosphatidylin-ositol-3-kinase, PI3K)/蛋白激酶B(protein kinase B, PKB,又称 Akt) 信号通路的作用. 结果显示: 随着 OBC 颗粒染毒质量浓度的增加 (5、10、20、40 µg/mL), 细胞内线粒体跨膜电位 (mitochondrial membrane potential, MMP) 水平逐渐下降, DNA 损伤程度逐渐升高, 呈现质量浓度和时间依赖性; 细胞外泌白细胞介素-4 (interleukin-4, IL-4) 水平升高和细胞内肿瘤坏死因子-α (tumor necrosis factor-α, TNF-α)基因高表达, 说明 OBC 颗粒会促进 SH-SY5Y 细胞发生炎症反应; 细胞内活性氧 (reactive oxygen species, ROS) 水平升高, 超氧化物歧化酶 (superoxide dismutase, SOD)、血红素加氧酶-1 (heme oxygenase-1, HO-1) 基因表达量升高, 且 HO-1 蛋白水平升高, 说明细胞发生氧化应激; 胞内 NF-κB 和 PI3K/Akt 通路相关蛋白显著变化, 表明 OBC 颗粒激活了 NF-κB和 PI3K/Akt 信号通路. 综上, OBC 颗粒可诱导 SH-SY5Y 细胞发生氧化应激造成 DNA 损伤, 促进炎症反应, 且对 NF-κB 和 PI3K/Akt 信号通路有重要调控作用.

关键词: 黑碳颗粒, SH-SY5Y 细胞, 炎症反应, 核因子-κB

Abstract: Human neuroblastoma cell SH-SY5Y was applied as a cell line model in order to explore its inflammatory responses to ozone oxidized black carbon (OBC) and also to investigate the potential roles of the nuclear factor-κB (NF-κB) and phosphatidylin-ositol- 3-kinase/protein kinase B (PI3K/Akt) pathways. The results showed that mitochondrial membrane potential (MMP) decreased and the degree of DNA damage increased signifi-cantly in a time- and concentration-dependent manner in SH-SY5Y cells after treatment with OBC. Interleukin-4 (IL-4) leakage and the expression of tumor necrosis factor-α (TNF-α)mRNA were found to increase concentration-dependently, suggesting that OBC could lead to inflammatory responses in SH-SY5Y cells. Meanwhile, significantly elevated in-tracellular reactive oxygen species (ROS) levels and the mRNA expression of superoxide dismutase (SOD) and heme oxygenase-1 (HO-1) demonstrated that OBC caused oxidative stress in SH-SY5Y cells. OBC activated the NF-κB and PI3K/Akt pathways, indicated by significant changes seen in certain proteins. In summary, the NF-κB and PI3K/Akt pathways probably played important roles in OBC promoted oxidative stress and the in-flammatory responses seen in SH-SY5Y cells.

Key words: black carbon (BC), SH-SY5Y cells, in?ammatory responses, nuclear factor-κB (NF-κB)

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