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Low-Dose Exposure of Silica Nanoparticles Induces Neurotoxicity via Neuroactive Ligand-Receptor Interaction Signaling Pathway in Zebrafish Embryos.
International Journal of Nanomedicine ( IF 6.6 ) Pub Date : 2020-06-19 , DOI: 10.2147/ijn.s254480 Jialiu Wei 1 , Jianhui Liu 2 , Shuang Liang 2 , Mengqi Sun 2 , Junchao Duan 2
International Journal of Nanomedicine ( IF 6.6 ) Pub Date : 2020-06-19 , DOI: 10.2147/ijn.s254480 Jialiu Wei 1 , Jianhui Liu 2 , Shuang Liang 2 , Mengqi Sun 2 , Junchao Duan 2
Affiliation
Objective: Silica nanoparticles (SiO2 NPs) have been extensively employed in biomedical field. SiO2 NPs are primarily designed to enter the circulatory system; however, little information is available on potential adverse effects of SiO2 NPs on the nervous system.
Methods: The neurotoxicity of SiO2 NPs at different concentrations (3, 6, 12 ng/nL) on zebrafish embryos was determined using immunofluorescence and microarray techniques, and subsequently confirmed by qRT-PCR.
Results: SiO2 NPs disrupt the axonal integrity and decrease the length of axons in Tg (NBT: EGFP) transgenic lines. The number of apoptotic cells in the brain and central nervous system of zebrafish embryos was increased in the presence of 12 ng/nL of SiO2 NPs, but the difference did not reach statistical significance. Screening for changes in the expression of genes involved in the neuroactive ligand–receptor interaction pathway was performed by microarray and confirmed by qRT-PCR. These analyses demonstrated that SiO2 NPs markedly downregulated genes associated with neural function (grm6a, drd1b, chrnb3b, adrb2a, grin2ab, npffr2.1, npy8br, gabrd, chrma3, gabrg3, gria3a, grm1a, adra2b, and glra3).
Conclusion: The obtained results documented that SiO2 NPs can induce developmental neurotoxicity by affecting the neuroactive ligand–receptor interaction signaling pathway. This new evidence may help to clarify the mechanism of SiO2 NPs-mediated neurotoxicity.
Keywords: silica nanoparticles, neurotoxicity, neuroactive ligand–receptor interaction signaling pathway, zebrafish
中文翻译：
二氧化硅纳米颗粒的低剂量暴露通过斑马鱼胚胎中的神经活性配体-受体相互作用信号通路诱导神经毒性。
目的：二氧化硅纳米粒子（SiO 2 NPs）已广泛应用于生物医学领域。SiO 2 NPs 主要设计用于进入循环系统；然而，关于 SiO 2 NPs 对神经系统的潜在不利影响的信息很少。
方法：使用免疫荧光和微阵列技术确定不同浓度（3、6、12 ng/nL）的 SiO 2 NPs 对斑马鱼胚胎的神经毒性，随后通过 qRT-PCR 确认。
结果： SiO 2NPs 破坏轴突完整性并减少 Tg (NBT: EGFP) 转基因系中轴突的长度。在12 ng/nL的SiO 2 NPs存在下，斑马鱼胚胎脑和中枢神经系统的凋亡细胞数量增加，但差异没有达到统计学意义。通过微阵列筛选参与神经活性配体 - 受体相互作用途径的基因表达变化，并通过 qRT-PCR 确认。这些分析表明，SiO 2 NPs 显着下调与神经功能相关的基因（grm6a、drd1b、chrnb3b、adrb2a、grin2ab、npffr2.1、npy8br、gabrd、chrma3、gabrg3、gria3a、grm1a、adra2b 和 glra3）。
结论：获得的结果表明，SiO 2NPs可以通过影响神经活性配体-受体相互作用信号通路诱导发育神经毒性。这一新证据可能有助于阐明 SiO 2 NPs 介导的神经毒性机制。
关键词：二氧化硅纳米粒子，神经毒性，神经活性配体-受体相互作用信号通路，斑马鱼
更新日期：2020-06-30
Methods: The neurotoxicity of SiO2 NPs at different concentrations (3, 6, 12 ng/nL) on zebrafish embryos was determined using immunofluorescence and microarray techniques, and subsequently confirmed by qRT-PCR.
Results: SiO2 NPs disrupt the axonal integrity and decrease the length of axons in Tg (NBT: EGFP) transgenic lines. The number of apoptotic cells in the brain and central nervous system of zebrafish embryos was increased in the presence of 12 ng/nL of SiO2 NPs, but the difference did not reach statistical significance. Screening for changes in the expression of genes involved in the neuroactive ligand–receptor interaction pathway was performed by microarray and confirmed by qRT-PCR. These analyses demonstrated that SiO2 NPs markedly downregulated genes associated with neural function (grm6a, drd1b, chrnb3b, adrb2a, grin2ab, npffr2.1, npy8br, gabrd, chrma3, gabrg3, gria3a, grm1a, adra2b, and glra3).
Conclusion: The obtained results documented that SiO2 NPs can induce developmental neurotoxicity by affecting the neuroactive ligand–receptor interaction signaling pathway. This new evidence may help to clarify the mechanism of SiO2 NPs-mediated neurotoxicity.
Keywords: silica nanoparticles, neurotoxicity, neuroactive ligand–receptor interaction signaling pathway, zebrafish
中文翻译：
二氧化硅纳米颗粒的低剂量暴露通过斑马鱼胚胎中的神经活性配体-受体相互作用信号通路诱导神经毒性。
目的：二氧化硅纳米粒子（SiO 2 NPs）已广泛应用于生物医学领域。SiO 2 NPs 主要设计用于进入循环系统；然而，关于 SiO 2 NPs 对神经系统的潜在不利影响的信息很少。
方法：使用免疫荧光和微阵列技术确定不同浓度（3、6、12 ng/nL）的 SiO 2 NPs 对斑马鱼胚胎的神经毒性，随后通过 qRT-PCR 确认。
结果： SiO 2NPs 破坏轴突完整性并减少 Tg (NBT: EGFP) 转基因系中轴突的长度。在12 ng/nL的SiO 2 NPs存在下，斑马鱼胚胎脑和中枢神经系统的凋亡细胞数量增加，但差异没有达到统计学意义。通过微阵列筛选参与神经活性配体 - 受体相互作用途径的基因表达变化，并通过 qRT-PCR 确认。这些分析表明，SiO 2 NPs 显着下调与神经功能相关的基因（grm6a、drd1b、chrnb3b、adrb2a、grin2ab、npffr2.1、npy8br、gabrd、chrma3、gabrg3、gria3a、grm1a、adra2b 和 glra3）。
结论：获得的结果表明，SiO 2NPs可以通过影响神经活性配体-受体相互作用信号通路诱导发育神经毒性。这一新证据可能有助于阐明 SiO 2 NPs 介导的神经毒性机制。
关键词：二氧化硅纳米粒子，神经毒性，神经活性配体-受体相互作用信号通路，斑马鱼
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