Ameliorative Effects by Hexagonal Boron Nitride Nanoparticles against Beta Amyloid Induced Neurotoxicity
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...
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MDPI AG
2022-08-01
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| Series: | Nanomaterials |
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| Online Access: | https://www.mdpi.com/2079-4991/12/15/2690 |
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| author | Nursah Aydin Hasan Turkez Ozlem Ozdemir Tozlu Mehmet Enes Arslan Mehmet Yavuz Erdal Sonmez Ozgur Fırat Ozpolat Ivana Cacciatore Antonio Di Stefano Adil Mardinoglu |
| author_facet | Nursah Aydin Hasan Turkez Ozlem Ozdemir Tozlu Mehmet Enes Arslan Mehmet Yavuz Erdal Sonmez Ozgur Fırat Ozpolat Ivana Cacciatore Antonio Di Stefano Adil Mardinoglu |
| author_sort | Nursah Aydin |
| collection | DOAJ |
| description | 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<sub>1-42</sub>) 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<sub>1-42</sub>-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<sub>1-42</sub> significantly decreased the rates of viable cells which was accompanied by elevated TOS level. Aβ<sub>1-42</sub> 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 (<i>p</i> < 0.05). All the Aβ<sub>1-42</sub>-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<sub>1-42</sub> 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. |
| first_indexed | 2024-03-09T05:07:56Z |
| format | Article |
| id | doaj.art-4ac967ef648c4ac28be3bca492e1b4d2 |
| institution | Directory Open Access Journal |
| issn | 2079-4991 |
| language | English |
| last_indexed | 2024-03-09T05:07:56Z |
| publishDate | 2022-08-01 |
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| record_format | Article |
| series | Nanomaterials |
| spelling | doaj.art-4ac967ef648c4ac28be3bca492e1b4d22023-12-03T12:52:34ZengMDPI AGNanomaterials2079-49912022-08-011215269010.3390/nano12152690Ameliorative Effects by Hexagonal Boron Nitride Nanoparticles against Beta Amyloid Induced NeurotoxicityNursah Aydin0Hasan Turkez1Ozlem Ozdemir Tozlu2Mehmet Enes Arslan3Mehmet Yavuz4Erdal Sonmez5Ozgur Fırat Ozpolat6Ivana Cacciatore7Antonio Di Stefano8Adil Mardinoglu9Department of Molecular Biology and Genetics, Erzurum Technical University, Erzurum 25050, TurkeyDepartment of Medical Biology, Faculty of Medicine, Atatürk University, Erzurum 25240, TurkeyDepartment of Molecular Biology and Genetics, Erzurum Technical University, Erzurum 25050, TurkeyDepartment of Molecular Biology and Genetics, Erzurum Technical University, Erzurum 25050, TurkeyREEM Neuropsychiatry Clinics, İstanbul 34245, TurkeyDepartment of Nanoscience and Nanoengineering, Graduate School of Natural and Applied Sciences, Ataturk University, Erzurum 25240, TurkeyComputer Sciences Research and Application Center, Atatürk University, Erzurum 25240, TurkeyDepartment of Pharmacy, University “G. d’Annunzio” of Chieti-Pescara, Via dei Vestini, 31, 66100 Chieti Scalo, CH, ItalyDepartment of Pharmacy, University “G. d’Annunzio” of Chieti-Pescara, Via dei Vestini, 31, 66100 Chieti Scalo, CH, ItalyScience for Life Laboratory, KTH-Royal Institute of Technology, SE-17121 Stockholm, SwedenAlzheimer’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<sub>1-42</sub>) 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<sub>1-42</sub>-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<sub>1-42</sub> significantly decreased the rates of viable cells which was accompanied by elevated TOS level. Aβ<sub>1-42</sub> 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 (<i>p</i> < 0.05). All the Aβ<sub>1-42</sub>-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<sub>1-42</sub> 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.https://www.mdpi.com/2079-4991/12/15/2690Alzheimer’s diseasebeta amyloidhexagonal boron nitride nanoparticlesneurotoxicityneuroprotectionSHSY5Y cells |
| spellingShingle | Nursah Aydin Hasan Turkez Ozlem Ozdemir Tozlu Mehmet Enes Arslan Mehmet Yavuz Erdal Sonmez Ozgur Fırat Ozpolat Ivana Cacciatore Antonio Di Stefano Adil Mardinoglu Ameliorative Effects by Hexagonal Boron Nitride Nanoparticles against Beta Amyloid Induced Neurotoxicity Nanomaterials Alzheimer’s disease beta amyloid hexagonal boron nitride nanoparticles neurotoxicity neuroprotection SHSY5Y cells |
| title | Ameliorative Effects by Hexagonal Boron Nitride Nanoparticles against Beta Amyloid Induced Neurotoxicity |
| title_full | Ameliorative Effects by Hexagonal Boron Nitride Nanoparticles against Beta Amyloid Induced Neurotoxicity |
| title_fullStr | Ameliorative Effects by Hexagonal Boron Nitride Nanoparticles against Beta Amyloid Induced Neurotoxicity |
| title_full_unstemmed | Ameliorative Effects by Hexagonal Boron Nitride Nanoparticles against Beta Amyloid Induced Neurotoxicity |
| title_short | Ameliorative Effects by Hexagonal Boron Nitride Nanoparticles against Beta Amyloid Induced Neurotoxicity |
| title_sort | ameliorative effects by hexagonal boron nitride nanoparticles against beta amyloid induced neurotoxicity |
| topic | Alzheimer’s disease beta amyloid hexagonal boron nitride nanoparticles neurotoxicity neuroprotection SHSY5Y cells |
| url | https://www.mdpi.com/2079-4991/12/15/2690 |
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