槲皮素对氧化锌纳米颗粒暴露大鼠小脑的神经保护作用。

IF 3.6 Q2 MEDICINE, RESEARCH & EXPERIMENTAL

Tissue Barriers Pub Date : 2023-07-03 DOI:10.1080/21688370.2022.2115273

Shaimaa A Abdelrahman, Amal S El-Shal, Abeer A Abdelrahman, Ebtehal Zaid Hassen Saleh, Abeer A Mahmoud

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引用次数: 1

摘要

工程纳米材料在细胞和分子水平上诱发危险效应。我们研究了氧化锌纳米颗粒(ZnONPs)对小脑组织的神经毒性潜在的不同机制，并阐明了槲皮素补充剂的改善作用。将40只成年雄性白化大鼠分为对照组(I)、ZnONPs暴露组(II)和ZnONPs和槲皮素组(III)，测定氧化应激生物标志物(MDA和TOS)、抗氧化生物标志物(SOD、GSH、GR和TAC)、血清白细胞介素(IL-1β、IL-6、IL-8)和肿瘤坏死因子α (TNF-α)的含量。血清微rna (miRNA):实时定量聚合酶链反应(RT-QPCR)检测miRNA-21-5p、miRNA-122-5p、miRNA-125b-5p、miRNA-155-3p表达水平。小脑组织切片用苏木精、伊红和银染色，显微镜下观察。免疫组织化学检测Calbindin D28k、GFAP、BAX蛋白在小脑组织中的表达水平。槲皮素的补充降低了氧化应激生物标志物水平，改善了ZnONPs降低的抗氧化参数。在研究组之间未检测到GR活性的显著差异。ZnONPs显著提高了大鼠血清IL-1β、IL-6、IL-8和TNF-α水平，槲皮素提高了这一水平。ZnONPs组大鼠血清miRNA-21-5p、miRNA-122-5p、miRNA-125b-5p、miRNA-155-p表达水平显著升高，槲皮素处理组与对照组差异无统计学意义。ZnONPs显著损害小脑组织结构，降低calbindin D28k水平，增加BAX和GFAP表达。槲皮素的补充改善了小脑组织的凋亡、胶质瘤和钙结合蛋白水平的提高。结论:槲皮素可从细胞和分子角度改善ZnONPs所致的小脑神经毒性。缩写:NPs:纳米粒子，ROS:活性氧，ZnONPs:氧化锌纳米粒子，AgNPs:银纳米粒子，BBB:血脑屏障，ncRNAs:非编码RNA, miRNA:微RNA, DMSO:二甲亚砜，LPO:脂质过氧化，MDA:丙二醛，TBA:硫代巴比托酸，TOS:总氧化状态，ELISA:酶联免疫吸附试验，H2O2:过氧化氢，SOD:超氧化物歧化酶，GR:谷胱甘肽还原酶，TAC:总抗氧化能力，IL-1:白细胞介素-1,TNF:肿瘤坏死因子α， cDNA:互补DNA, RT-QPCR:实时定量聚合酶链反应，ABC:亲和素生物素复合物技术，DAB: 3'， 3-二氨基联苯胺，SPSS:社会科学统计包，ANOVA:单向方差分析，Tukey's HSD: Tukey's honest显著差异，GFAP:胶质纤维酸性蛋白，iNOS:诱导型一氧化氮合酶，NO:一氧化氮，HO-1:血红素氧化酶-1,Nrf2:核因子红系2相关因子2,NF-B:核因子- b, SCI:脊髓损伤，CB:钙结合蛋白。

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Neuroprotective effects of quercetin on the cerebellum of zinc oxide nanoparticles (ZnoNps)-exposed rats.

Engineered nanomaterials induce hazardous effects at the cellular and molecular levels. We investigated different mechanisms underlying the neurotoxic potential of zinc oxide nanoparticles (ZnONPs) on cerebellar tissue and clarified the ameliorative role of Quercetin supplementation. Forty adult male albino rats were divided into control group (I), ZnONPs-exposed group (II), and ZnONPs and Quercetin group (III). Oxidative stress biomarkers (MDA & TOS), antioxidant biomarkers (SOD, GSH, GR, and TAC), serum interleukins (IL-1β, IL-6, IL-8), and tumor necrosis factor alpha (TNF-α) were measured. Serum micro-RNA (miRNA): miRNA-21-5p, miRNA-122-5p, miRNA-125b-5p, and miRNA-155-3p expression levels were quantified by real-time quantitative polymerase-chain reaction (RT-QPCR). Cerebellar tissue sections were stained with Hematoxylin & Eosin and Silver stains and examined microscopically. Expression levels of Calbindin D28k, GFAP, and BAX proteins in cerebellar tissue were detected by immunohistochemistry. Quercetin supplementation lowered oxidative stress biomarkers levels and ameliorated the antioxidant parameters that were decreased by ZnONPs. No significant differences in GR activity were detected between the study groups. ZnONPs significantly increased serum IL-1β, IL-6, IL-8, and TNF-α which were improved with Quercetin. Serum miRNA-21-5p, miRNA-122-5p, miRNA-125b-5p, and miRNA-155-p expression levels showed significant increase in ZnONPs group, while no significant difference was observed between Quercetin-treated group and control group. ZnONPs markedly impaired cerebellar tissue structure with decreased levels of calbindin D28k, increased BAX and GFAP expression. Quercetin supplementation ameliorated cerebellar tissue apoptosis, gliosis and improved calbindin levels. In conclusion: Quercetin supplementation ameliorated cerebellar neurotoxicity induced by ZnONPs at cellular and molecular basis by different studied mechanisms.Abbreviations: NPs: Nanoparticles, ROS: reactive oxygen species, ZnONPs: Zinc oxide nanoparticles, AgNPs: silver nanoparticles, BBB: blood-brain barrier, ncRNAs: Non-coding RNAs, miRNA: Micro RNA, DMSO: Dimethyl sulfoxide, LPO: lipid peroxidation, MDA: malondialdehyde, TBA: thiobarbituric acid, TOS: total oxidative status, ELISA: enzyme-linked immunosorbent assay, H₂O₂: hydrogen peroxide, SOD: superoxide dismutase, GR: glutathione reductase, TAC: total antioxidant capacity, IL-1: interleukin-1, TNF: tumor necrosis factor alpha, cDNA: complementary DNA, RT-QPCR: Real-time quantitative polymerase-chain reaction, ABC: Avidin biotin complex technique, DAB: 3', 3-diaminobenzidine, SPSS: Statistical Package for Social Sciences, ANOVA: One way analysis of variance, Tukey's HSD: Tukey's Honestly Significant Difference, GFAP: glial fiberillar acitic protein, iNOS: Inducible nitric oxide synthase, NO: nitric oxide, HO-1: heme oxygenase-1, Nrf2: nuclear factor erythroid 2-related factor 2, NF-B: nuclear factor-B, SCI: spinal cord injury, CB: Calbindin.

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来源期刊

Tissue Barriers MEDICINE, RESEARCH & EXPERIMENTAL-

CiteScore

6.60

自引率

6.50%

发文量

期刊介绍： Tissue Barriers is the first international interdisciplinary journal that focuses on the architecture, biological roles and regulation of tissue barriers and intercellular junctions. We publish high quality peer-reviewed articles that cover a wide range of topics including structure and functions of the diverse and complex tissue barriers that occur across tissue and cell types, including the molecular composition and dynamics of polarized cell junctions and cell-cell interactions during normal homeostasis, injury and disease state. Tissue barrier formation in regenerative medicine and restoration of tissue and organ function is also of interest. Tissue Barriers publishes several categories of articles including: Original Research Papers, Short Communications, Technical Papers, Reviews, Perspectives and Commentaries, Hypothesis and Meeting Reports. Reviews and Perspectives/Commentaries will typically be invited. We also anticipate to publish special issues that are devoted to rapidly developing or controversial areas of research. Suggestions for topics are welcome. Tissue Barriers objectives: Promote interdisciplinary awareness and collaboration between researchers working with epithelial, epidermal and endothelial barriers and to build a broad and cohesive worldwide community of scientists interesting in this exciting field. Comprehend the enormous complexity of tissue barriers and map cross-talks and interactions between their different cellular and non-cellular components. Highlight the roles of tissue barrier dysfunctions in human diseases. Promote understanding and strategies for restoration of tissue barrier formation and function in regenerative medicine. Accelerate a search for pharmacological enhancers of tissue barriers as potential therapeutic agents. Understand and optimize drug delivery across epithelial and endothelial barriers.