Ameliorative Effects by Hexagonal Boron Nitride Nanoparticles against Beta Amyloid Induced Neurotoxicity.
Nursah AydinHasan TurkezOzlem Ozdemir TozluMehmet Enes ArslanMehmet YavuzErdal SonmezOzgur Fırat OzpolatIvana CacciatoreAntonio Di StefanoAdil MardingluPublished in: Nanomaterials (Basel, Switzerland) (2022)
Alzheimer's disease (AD) is considered as the most common neurodegenerative disease. Extracellular amyloid beta (Aβ) deposition is a hallmark of AD. The options based on degradation and clearance of Aβ 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 (Aβ 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). Aβ 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 Aβ 1-42 significantly decreased the rates of viable cells which was accompanied by elevated TOS level. Aβ 1-42 induced both apoptotic and necrotic cell death. Aβ exposure led to significant increases in expression levels of APOE, BACE 1, EGFR, NCTSN and TNF-α genes and significant decreases in expression levels of ADAM 10, APH1A, BDNF, PSEN1 and PSENEN genes ( p < 0.05). All the Aβ 1-42 -induced neurotoxic insults were inhibited by the applications with hBN-NPs. hBN-NPs also suppressed the remarkable elevation in the signal for Aβ following exposure to Aβ 1-42 for 48 h. Our results indicated that hBN-NPs could significantly prevent the neurotoxic damages by Aβ. Thus, hBN-NPs could be a novel and promising anti-AD agent for effective drug development, bio-nano imaging or drug delivery strategies.
Keyphrases
- electron microscopy
- cell death
- high glucose
- diabetic rats
- cell cycle arrest
- poor prognosis
- drug delivery
- endothelial cells
- oxide nanoparticles
- high resolution
- induced apoptosis
- small cell lung cancer
- drug induced
- oxidative stress
- genome wide
- mesenchymal stem cells
- magnetic resonance imaging
- early onset
- quantum dots
- high throughput
- dna methylation
- magnetic resonance
- gene expression
- high fat diet
- cell therapy
- adipose tissue
- bone marrow
- stress induced
- anti inflammatory