Related Experiment Video
Updated: Apr 22, 2026
Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
Published on: October 30, 2018
Paeoniflorin attenuates Aβ25-35-induced neurotoxicity in PC12 cells by preventing mitochondrial dysfunction
Jialei Li1, Xiaoxia Ji, Jianping Zhang
1Jialei Li, Department of Internal Neurology, Wuxi People's Hospital, Wuxi, Jiangsu Province, China, phone: +86 13912489660, fax: (00) 86-(0) 510-85520770,
Abstract:
The pathogenic mechanism of neurodegenerative brain disorder such as Alzheimer's disease (AD) has been still far from clearly understood. Previous research has identified that mitochondrial dysfunction induced by Aβ has been recognized as a hallmark in AD. Therefore, the effective agents targeting β-amyloid (Aβ)-induced mitochondrial dysfunction may be useful for the treatment or prevention of AD. In the present study, the neuroprotective effect of paeoniflorin (PF), one monoterpene glycoside isolated from the Chinese herb Radix Paeoniae alba, on Aβ25-35-induced toxicity in PC12 cells was investigated for the first time. The results showed that PF could attenuate or restore the cell injury induced by Aβ25-35 in PC12 cells through preventing mitochondrial dysfunction, including decreased mitochondrial membrane potential, increased cytochrome c release as well as activity of caspase-3 and caspase-9. Therefore, our data provide the evidence that PF could protect PC12 cells against Aβ25-35-induced neurotoxicity and might be a potentially therapeutic approach for AD in the future.
Insights
Paeoniflorin (PF) protects against Alzheimer's disease (AD) by preventing mitochondrial dysfunction caused by amyloid-beta (Aβ). This natural compound may offer a future therapeutic strategy for AD treatment.
Area of Science:
- Neuroscience
- Pharmacology
- Cell Biology
Background:
- Alzheimer's disease (AD) pathogenesis remains unclear, with amyloid-beta (Aβ)-induced mitochondrial dysfunction identified as a key feature.
- Targeting Aβ-induced mitochondrial dysfunction presents a potential therapeutic avenue for AD.
Purpose of the Study:
- To investigate the neuroprotective effects of paeoniflorin (PF) against Aβ25-35-induced toxicity in PC12 cells.
- To explore PF's mechanism in preventing mitochondrial dysfunction in an AD cellular model.
Main Methods:
- PC12 cells were treated with Aβ25-35 to induce neurotoxicity.
- The effects of paeoniflorin (PF) on cell viability and mitochondrial function were assessed.
- Mitochondrial membrane potential, cytochrome c release, and caspase activity were measured.
Main Results:
- Paeoniflorin (PF) attenuated Aβ25-35-induced cell injury in PC12 cells.
- PF prevented the decrease in mitochondrial membrane potential caused by Aβ25-35.
- PF inhibited Aβ25-35-induced release of cytochrome c and activation of caspase-3 and caspase-9.
Conclusions:
- Paeoniflorin (PF) demonstrates neuroprotective effects against Aβ25-35-induced neurotoxicity in PC12 cells.
- PF protects cells by preventing mitochondrial dysfunction, including maintaining mitochondrial membrane potential and inhibiting apoptosis.
- PF shows potential as a therapeutic agent for Alzheimer's disease.
