首页|短链氯化石蜡通过ROS/NF-κB通路诱导PC12细胞神经毒性

短链氯化石蜡通过ROS/NF-κB通路诱导PC12细胞神经毒性

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目的:研究短链氯化石蜡(SCCPs)神经毒性机制.方法:显微镜下观察和CCK-8检测SCCPs不同浓度(0、50、100、200、300 μg/L)暴露24 h的PC12细胞的生长密度和细胞活力;活性氧(ROS)和丙二醛(MDA)检测细胞氧化损伤情况;Western blot检测iNOS、COX-2、p65、p-p65蛋白表达;qRT-PCR检测IL-1β、IL-6、TNF-α炎症因子转录水平.结果:显微镜观察和CCK-8结果显示PC12细胞的密度和细胞活力在200 μg/L SCCPs暴露时降低(P<0.01),细胞内ROS和MDA相对水平在200 µg/L SCCPs暴露时升高(P<0.001).N-乙酰半胱氨酸(NAC)干预下,NF-κB通路相关蛋白和mRNA表达被抑制(P<0.05).结论:SCCPs可通过ROS/NF-κB通路诱导PC12细胞神经毒性.
Short-chain chlorinated paraffins inducing neurotoxicity in PC 12 cells through the ROS/NF-κB pathway
Objective:To investigate the neurotoxic mechanism of short-chain chlorinated paraffins(SCCPs).Methods:PC12 cells were initially exposed to SCCPs at different concentrations(0,50,100,200,300 μg/L,respectively)for 24 hours,and then observed under a microscope and assayed using CCK-8 for their growth density and viability.Reactive oxygen species(ROS)and malondialdehyde(MDA)were used to detect cellular oxidative damage.Western blot was conducted to detect the protein expression of iNOS,COX-2,p65 and p-p65.qRT-PCR was used to detect the transcription levels of inflammatory cytokines IL-1 β,IL-6,and TNF-α.Results:Microscopy and CCK-8 analysis results showed that the density and viability of PC 12 cells were decreased upon exposing to 200 μg/L SCCPs(P<0.01),and the relative levels of intracellular ROS and MDA were increased under the same exposure conditions(P<0.001).Under NAC intervention,the expression of NF-κB pathway-related proteins and mRNAs was inhibited(P<0.05).Conclusion:SCCPs can induce neurotoxicity in PC12 cell via ROS/NF-κB pathway.

short-chain chlorinated paraffinsneurotoxicityROS/NF-κB pathway

张涛、伏家林、王若薇、胡名媛、余越、许淼、周钰睿、方正美、陈燕

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皖南医学院 公共卫生学院慢性病防制研究所,安徽 芜湖 241002

短链氯化石蜡 神经毒性 ROS/NF-κB通路

安徽高校自然科学研究项目皖南医学院中青年科研基金项目

KJ2021ZD0098WK2023ZQNZ12

2024

皖南医学院学报
皖南医学院

皖南医学院学报

CSTPCD
影响因子:0.695
ISSN:1002-0217
年,卷(期):2024.43(5)
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