Oxytocin Protects PC12 Cells Against β-Amyloid-Induced Cell Injury
<b>Background/Objectives</b>: Neurodegenerative diseases, particularly Alzheimer’s disease (AD), are characterized by progressive cognitive decline and non-cognitive symptoms that significantly affect health and quality of life. Beta-amyloid (Aβ) protein accumulation is a key factor in A...
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MDPI AG
2025-03-01
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| author | Mohammed Mufadhe Alanazi Awatif B. Albaker Lamia A. Alzaagi Jawza F. Alsabhan Fawaz Alasmari Mohammed M. Almutairi Metab S. Alharbi Abdullah F. Alasmari Faleh Alqahtani Sary Alsanea |
| author_facet | Mohammed Mufadhe Alanazi Awatif B. Albaker Lamia A. Alzaagi Jawza F. Alsabhan Fawaz Alasmari Mohammed M. Almutairi Metab S. Alharbi Abdullah F. Alasmari Faleh Alqahtani Sary Alsanea |
| author_sort | Mohammed Mufadhe Alanazi |
| collection | DOAJ |
| description | <b>Background/Objectives</b>: Neurodegenerative diseases, particularly Alzheimer’s disease (AD), are characterized by progressive cognitive decline and non-cognitive symptoms that significantly affect health and quality of life. Beta-amyloid (Aβ) protein accumulation is a key factor in AD pathology, leading to neuronal damage. Oxytocin (OXT), a neuropeptide with neuroprotective potential, has garnered interest owing to its ability to mitigate neurotoxicity. We hypothesized that oxytocin could protect PC12 cells from Aβ-induced cytotoxicity through antioxidant effects and modulation of apoptotic pathways (i.e., mitochondrial and MAPK pathways). In this study, we aim to assess oxytocin’s protective effects on cell viability, oxidative stress, mitochondrial function, and apoptotic signaling. <b>Methods</b>: PC12 cells were treated with Aβ25–35 and pre-treated with varying oxytocin concentrations to assess cell viability, reactive oxygen species (ROS) generation, and mitochondrial membrane potential. Western blotting was performed to analyze the effects on mitochondrial apoptosis and MAPK pathways. <b>Results</b>: Oxytocin treatment significantly improved cell viability in a dose-dependent manner and reduced Aβ-induced oxidative stress and mitochondrial dysfunction. Oxytocin-treated groups exhibited decreased ROS levels, increased mitochondrial membrane potential, and modulation of apoptosis-related proteins. Oxytocin upregulated phosphorylated ERK1/2 and Bcl-2 while downregulating BAX and caspase-3, reducing the BAX/Bcl-2 ratio. <b>Conclusions</b>: Oxytocin effectively protects PC12 cells from Aβ-induced neurotoxicity, highlighting its potential as a therapeutic agent for AD. Further research is needed to clarify oxytocin’s mechanisms and clinical implications in AD treatment. |
| format | Article |
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| institution | Kabale University |
| issn | 1424-8247 |
| language | English |
| publishDate | 2025-03-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Pharmaceuticals |
| spelling | doaj-art-3f61de4a495c4ec888d0b97d92a1d6eb2025-08-20T03:43:26ZengMDPI AGPharmaceuticals1424-82472025-03-0118339010.3390/ph18030390Oxytocin Protects PC12 Cells Against β-Amyloid-Induced Cell InjuryMohammed Mufadhe Alanazi0Awatif B. Albaker1Lamia A. Alzaagi2Jawza F. Alsabhan3Fawaz Alasmari4Mohammed M. Almutairi5Metab S. Alharbi6Abdullah F. Alasmari7Faleh Alqahtani8Sary Alsanea9Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi ArabiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi ArabiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi ArabiaDepartment of Clinical Pharmacy, College of Pharmacy, King Saud University, Riyadh 11451, Saudi ArabiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi ArabiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi ArabiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi ArabiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi ArabiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi ArabiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia<b>Background/Objectives</b>: Neurodegenerative diseases, particularly Alzheimer’s disease (AD), are characterized by progressive cognitive decline and non-cognitive symptoms that significantly affect health and quality of life. Beta-amyloid (Aβ) protein accumulation is a key factor in AD pathology, leading to neuronal damage. Oxytocin (OXT), a neuropeptide with neuroprotective potential, has garnered interest owing to its ability to mitigate neurotoxicity. We hypothesized that oxytocin could protect PC12 cells from Aβ-induced cytotoxicity through antioxidant effects and modulation of apoptotic pathways (i.e., mitochondrial and MAPK pathways). In this study, we aim to assess oxytocin’s protective effects on cell viability, oxidative stress, mitochondrial function, and apoptotic signaling. <b>Methods</b>: PC12 cells were treated with Aβ25–35 and pre-treated with varying oxytocin concentrations to assess cell viability, reactive oxygen species (ROS) generation, and mitochondrial membrane potential. Western blotting was performed to analyze the effects on mitochondrial apoptosis and MAPK pathways. <b>Results</b>: Oxytocin treatment significantly improved cell viability in a dose-dependent manner and reduced Aβ-induced oxidative stress and mitochondrial dysfunction. Oxytocin-treated groups exhibited decreased ROS levels, increased mitochondrial membrane potential, and modulation of apoptosis-related proteins. Oxytocin upregulated phosphorylated ERK1/2 and Bcl-2 while downregulating BAX and caspase-3, reducing the BAX/Bcl-2 ratio. <b>Conclusions</b>: Oxytocin effectively protects PC12 cells from Aβ-induced neurotoxicity, highlighting its potential as a therapeutic agent for AD. Further research is needed to clarify oxytocin’s mechanisms and clinical implications in AD treatment.https://www.mdpi.com/1424-8247/18/3/390Alzheimer’s diseaseoxytocinPC12 cellsβ-amyloid proteinBcl-2BAX |
| spellingShingle | Mohammed Mufadhe Alanazi Awatif B. Albaker Lamia A. Alzaagi Jawza F. Alsabhan Fawaz Alasmari Mohammed M. Almutairi Metab S. Alharbi Abdullah F. Alasmari Faleh Alqahtani Sary Alsanea Oxytocin Protects PC12 Cells Against β-Amyloid-Induced Cell Injury Pharmaceuticals Alzheimer’s disease oxytocin PC12 cells β-amyloid protein Bcl-2 BAX |
| title | Oxytocin Protects PC12 Cells Against β-Amyloid-Induced Cell Injury |
| title_full | Oxytocin Protects PC12 Cells Against β-Amyloid-Induced Cell Injury |
| title_fullStr | Oxytocin Protects PC12 Cells Against β-Amyloid-Induced Cell Injury |
| title_full_unstemmed | Oxytocin Protects PC12 Cells Against β-Amyloid-Induced Cell Injury |
| title_short | Oxytocin Protects PC12 Cells Against β-Amyloid-Induced Cell Injury |
| title_sort | oxytocin protects pc12 cells against β amyloid induced cell injury |
| topic | Alzheimer’s disease oxytocin PC12 cells β-amyloid protein Bcl-2 BAX |
| url | https://www.mdpi.com/1424-8247/18/3/390 |
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