Inhibition of Glycogen Synthase Kinase and the Neuroprotective Function of Conjugated ZnO-Osthol Nanoparticles in Alzheimer’s Disease
A critical factor in the cause and progression of Alzheimer’s disease (AD) is the growth of β-amyloid peptide (Aβ) in the brain. The mechanism of this effect is still unknown, although the effect of osthol on Aβ-induced inflammation is neuroprotective in AD and supplementation with zinc might preven...
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| Format: | Article |
| Language: | English |
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Wiley
2022-01-01
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| Series: | Bioinorganic Chemistry and Applications |
| Online Access: | http://dx.doi.org/10.1155/2022/1401995 |
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| author | Nahed S. Alharthi Fahad M. Aldakheel Abdulkarim S. Binshaya |
| author_facet | Nahed S. Alharthi Fahad M. Aldakheel Abdulkarim S. Binshaya |
| author_sort | Nahed S. Alharthi |
| collection | DOAJ |
| description | A critical factor in the cause and progression of Alzheimer’s disease (AD) is the growth of β-amyloid peptide (Aβ) in the brain. The mechanism of this effect is still unknown, although the effect of osthol on Aβ-induced inflammation is neuroprotective in AD and supplementation with zinc might prevent or delay the onset of dementia. In the current study, by inducing APP vector in human BE (2)-M17 cells, we established a cellular model of AD and investigated the protective effect of osthol (7-methoxy-8-3-methyl-2-butenyl-2H-1-benzopyran-2-one)-zinc oxide nanoparticles. The osthol-conjugated zinc oxide nanoparticles could significantly increase cell viability by inhibiting cell apoptosis. Osthol treatment has also prevented synaptic proteins such as postsynaptic density-95 (PSD-95), synaptophysin (SYP), and synapsin-1 from decreasing in APP-induced BE (2)-M17 cells. In addition, the expression of miR-132 was significantly upregulated by osthol by triggering the Wnt/β-catenin signaling pathway. We conclude from our observations that osthol is a potential drug for the treatment of a neurodegenerative disease, Alzheimer’s. The key reason was that by upregulating miR-132, osthol could inhibit APP expression to prevent AD from occurring. |
| format | Article |
| id | doaj-art-6ab4daa858af4c2da4d9b2363f0572ae |
| institution | Kabale University |
| issn | 1687-479X |
| language | English |
| publishDate | 2022-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Bioinorganic Chemistry and Applications |
| spelling | doaj-art-6ab4daa858af4c2da4d9b2363f0572ae2025-02-03T10:59:56ZengWileyBioinorganic Chemistry and Applications1687-479X2022-01-01202210.1155/2022/1401995Inhibition of Glycogen Synthase Kinase and the Neuroprotective Function of Conjugated ZnO-Osthol Nanoparticles in Alzheimer’s DiseaseNahed S. Alharthi0Fahad M. Aldakheel1Abdulkarim S. Binshaya2Department of Medical Laboratory SciencesDepartment of Clinical Laboratory SciencesDepartment of Medical Laboratory SciencesA critical factor in the cause and progression of Alzheimer’s disease (AD) is the growth of β-amyloid peptide (Aβ) in the brain. The mechanism of this effect is still unknown, although the effect of osthol on Aβ-induced inflammation is neuroprotective in AD and supplementation with zinc might prevent or delay the onset of dementia. In the current study, by inducing APP vector in human BE (2)-M17 cells, we established a cellular model of AD and investigated the protective effect of osthol (7-methoxy-8-3-methyl-2-butenyl-2H-1-benzopyran-2-one)-zinc oxide nanoparticles. The osthol-conjugated zinc oxide nanoparticles could significantly increase cell viability by inhibiting cell apoptosis. Osthol treatment has also prevented synaptic proteins such as postsynaptic density-95 (PSD-95), synaptophysin (SYP), and synapsin-1 from decreasing in APP-induced BE (2)-M17 cells. In addition, the expression of miR-132 was significantly upregulated by osthol by triggering the Wnt/β-catenin signaling pathway. We conclude from our observations that osthol is a potential drug for the treatment of a neurodegenerative disease, Alzheimer’s. The key reason was that by upregulating miR-132, osthol could inhibit APP expression to prevent AD from occurring.http://dx.doi.org/10.1155/2022/1401995 |
| spellingShingle | Nahed S. Alharthi Fahad M. Aldakheel Abdulkarim S. Binshaya Inhibition of Glycogen Synthase Kinase and the Neuroprotective Function of Conjugated ZnO-Osthol Nanoparticles in Alzheimer’s Disease Bioinorganic Chemistry and Applications |
| title | Inhibition of Glycogen Synthase Kinase and the Neuroprotective Function of Conjugated ZnO-Osthol Nanoparticles in Alzheimer’s Disease |
| title_full | Inhibition of Glycogen Synthase Kinase and the Neuroprotective Function of Conjugated ZnO-Osthol Nanoparticles in Alzheimer’s Disease |
| title_fullStr | Inhibition of Glycogen Synthase Kinase and the Neuroprotective Function of Conjugated ZnO-Osthol Nanoparticles in Alzheimer’s Disease |
| title_full_unstemmed | Inhibition of Glycogen Synthase Kinase and the Neuroprotective Function of Conjugated ZnO-Osthol Nanoparticles in Alzheimer’s Disease |
| title_short | Inhibition of Glycogen Synthase Kinase and the Neuroprotective Function of Conjugated ZnO-Osthol Nanoparticles in Alzheimer’s Disease |
| title_sort | inhibition of glycogen synthase kinase and the neuroprotective function of conjugated zno osthol nanoparticles in alzheimer s disease |
| url | http://dx.doi.org/10.1155/2022/1401995 |
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