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Ameliorative Effects by Hexagonal Boron Nitride Nanoparticles against Beta Amyloid Induced Neurotoxicity
Erzurum Tech Univ, Dept Mol Biol & Genet, TR-25050 Erzurum, Turkey..
Ataturk Univ, Fac Med, Dept Med Biol, TR-25240 Erzurum, Turkey.;Ataturk Univ, East Anatolia High Technol Applicat & Res Ctr DAY, TR-25240 Erzurum, Turkey..
Erzurum Tech Univ, Dept Mol Biol & Genet, TR-25050 Erzurum, Turkey..
Erzurum Tech Univ, Dept Mol Biol & Genet, TR-25050 Erzurum, Turkey..ORCID iD: 0000-0002-1600-2305
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2022 (English)In: Nanomaterials, E-ISSN 2079-4991, Vol. 12, no 15, p. 2690-, article id 2690Article in journal (Refereed) Published
Abstract [en]

Alzheimer's disease (AD) is considered as the most common neurodegenerative disease. Extracellular amyloid beta (A beta) deposition is a hallmark of AD. The options based on degradation and clearance of A beta are preferred as promising therapeutic strategies for AD. Interestingly, recent findings indicate that boron nanoparticles not only act as a carrier but also play key roles in mediating biological effects. In the present study, the aim was to investigate the effects of different concentrations (0-500 mg/L) of hexagonal boron nitride nanoparticles (hBN-NPs) against neurotoxicity by beta amyloid (A beta(1-42)) in differentiated human SH-SY5Y neuroblastoma cell cultures for the first time. The synthesized hBN-NPs were characterized by X-ray diffraction (XRD) measurements, scanning electron microscopy (SEM) and transmission electron microscopy (TEM). A beta(1-42)-induced neurotoxicity and therapeutic potential by hBN-NPs were assessed on differentiated SH-SY5Y cells using MTT and LDH release assays. Levels of total antioxidant capacity (TAC) and total oxidant status (TOS), expression levels of genes associated with AD and cellular morphologies were examined. The exposure to A beta(1-42) significantly decreased the rates of viable cells which was accompanied by elevated TOS level. A beta(1-42) induced both apoptotic and necrotic cell death. A beta exposure led to significant increases in expression levels of APOE, BACE 1, EGFR, NCTSN and TNF-alpha genes and significant decreases in expression levels of ADAM 10, APH1A, BDNF, PSEN1 and PSENEN genes (p < 0.05). All the A beta(1-42)-induced neurotoxic insults were inhibited by the applications with hBN-NPs. hBN-NPs also suppressed the remarkable elevation in the signal for A beta following exposure to A beta(1-42) for 48 h. Our results indicated that hBN-NPs could significantly prevent the neurotoxic damages by A beta. Thus, hBN-NPs could be a novel and promising anti-AD agent for effective drug development, bio-nano imaging or drug delivery strategies.

Place, publisher, year, edition, pages
2022. Vol. 12, no 15, p. 2690-, article id 2690
Keywords [en]
Alzheimer's disease, beta amyloid, hexagonal boron nitride nanoparticles, neurotoxicity, neuroprotection, SHSY5Y cells, in vitro
National Category
Pediatrics Occupational Health and Environmental Health Neurology
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URN: urn:nbn:se:kth:diva-316790DOI: 10.3390/nano12152690ISI: 000839814500001PubMedID: 35957121Scopus ID: 2-s2.0-85136913274OAI: oai:DiVA.org:kth-316790DiVA, id: diva2:1691332
Note

QC 20220830

Available from: 2022-08-30 Created: 2022-08-30 Last updated: 2023-05-15Bibliographically approved

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Mardinoglu, Adil

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