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Protective effect of paeoniflorin on Aβ25-35-induced SH-SY5Y cell injury by preventing mitochondrial dysfunction
1Key Laboratory of Nuclear Medicine, Ministry of Health, Jiangsu Key Laboratory of Molecular Nuclear Medicine, Jiangsu Institute of Nuclear Medicine, Wuxi, 214063, Jiangsu Province, China, nypd0723@gmail.com.
Abstract:
Alzheimer's disease (AD) is a major neurodegenerative brain disorder affecting about 14 million people worldwide. Aβ-induced cell injury is a crucial cause of neuronal loss in AD, thus the suppression of which might be useful for the treatment of this disease. In this study, we aimed to evaluate the effect of paeoniflorin (PF), a monoterpene glycoside isolated from aqueous extract of Radix Paeoniae Alba, on Aβ25-35-induced cytotoxicity in SH-SY5Y cells. The results showed PF could attenuate or restore the viability loss, apoptotic increase, and ROS production induced by Aβ25-35 in SH-SY5Y cells. In addition, PF strikingly inhibited Aβ25-35-induced mitochondrial dysfunction, which includes decreased mitochondrial membrane potential, increased Bax/Bcl-2 ratio, cytochrome c release and activity of caspase-3 and caspase-9. Therefore, our study provided the first experimental evidence that PF could modulate ROS production and apoptotic mitochondrial pathway in model of neuron injury in vitro and which might provide new insights into its application toward Alzheimer's disease therapy.
Insights
Paeoniflorin (PF) protects against amyloid-beta-induced neurotoxicity in Alzheimer's disease models. This compound reduces cell death, oxidative stress, and mitochondrial dysfunction, offering potential therapeutic benefits for Alzheimer's disease.
Area of Science:
- Neuroscience
- Pharmacology
- Cell Biology
Background:
- Alzheimer's disease (AD) is a leading cause of neurodegeneration, characterized by neuronal loss.
- Amyloid-beta (Aβ) peptide-induced cytotoxicity is a key factor contributing to neuronal damage in AD.
- Developing effective treatments to counteract Aβ toxicity is crucial for managing Alzheimer's disease.
Purpose of the Study:
- To investigate the neuroprotective effects of paeoniflorin (PF) against Aβ25-35-induced cytotoxicity.
- To evaluate PF's impact on cell viability, apoptosis, and reactive oxygen species (ROS) production in neuronal cells.
- To examine PF's influence on mitochondrial dysfunction and related apoptotic pathways.
Main Methods:
- Utilized SH-SY5Y human neuroblastoma cells as an in vitro model.
- Induced cytotoxicity using the Aβ25-35 peptide fragment.
- Assessed cell viability, apoptosis markers (Bax/Bcl-2 ratio, caspase activity), mitochondrial membrane potential, and ROS levels.
- Administered paeoniflorin (PF) derived from Radix Paeoniae Alba.
Main Results:
- Paeoniflorin (PF) significantly attenuated Aβ25-35-induced loss of cell viability.
- PF reduced Aβ25-35-induced apoptosis and reactive oxygen species (ROS) production.
- PF inhibited mitochondrial dysfunction, including restoring mitochondrial membrane potential and decreasing caspase-3 and caspase-9 activity.
- PF treatment modulated the Bax/Bcl-2 ratio and prevented cytochrome c release.
Conclusions:
- Paeoniflorin (PF) demonstrates significant neuroprotective effects against Aβ25-35-induced neuronal injury in vitro.
- PF mitigates neuronal damage by modulating ROS production and inhibiting the apoptotic mitochondrial pathway.
- These findings suggest paeoniflorin holds promise as a potential therapeutic agent for Alzheimer's disease.
