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  

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

作　　者：黄津 王田田 安静[1] 钟玉芳[1] 尚羽[1] HUANG Jin;WANG Tiantian;AN Jing;ZHONG Yufang;SHANG Yu(Institute of Environmental Pollution and Health,School of Environmental and Chemical Engineering,Shanghai University,Shanghai 200444,China)

机构地区：[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　　处：《上海大学学报（自然科学版）》2024年第2期218-228,共11页Journal of Shanghai University:Natural Science Edition

基　　金：国家自然科学面上基金资助项目(41977366)。

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、40µg/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.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-ositol3-kinase/protein kinase B(PI3K/Akt)pathways.The results showed that mitochondrial membrane potential(MMP)decreased and the degree of DNA damage increased significantly 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(TNFα)mRNA were found to increase concentration-dependently,suggesting that OBC could lead to inflammatory responses in SH-SY5Y cells.Meanwhile,significantly elevated intracellular 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 inflammatory responses seen in SH-SY5Y cells.

关 键 词：黑碳颗粒 SH-SY5Y细胞 炎症反应 核因子-ΚB 

分 类 号：X513[环境科学与工程—环境工程]