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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Main Authors: 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
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Language:English
Published: MDPI AG 2025-03-01
Series:Pharmaceuticals
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Online Access:https://www.mdpi.com/1424-8247/18/3/390
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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.
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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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