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TISSUE BARRIERS
Taylor& Francis
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Abstract: |
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.
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