Asiatic acid protects differentiated PC12 cells from Aβ25–35-induced apoptosis and tau hyperphosphorylation via regulating PI3K/Akt/GSK-3β signaling
Abstract
Amyloid β (Aβ) peptide can cause neurotoxicity in Alzheimer's disease (AD). The main purpose of the present study is to investigate the protective role of asiatic acid (AA) against Aβ 25-35-induced neurotoxicity in neuronally differentiated PC12 cells. Differentiated PC12 cells were pretreated with 5, 10 or 20 μM AA before treatment with 20 μM Aβ 25-35. The viability and apoptosis of differentiated PC12 cells were determined by MTT assay and Annexin V-FITC/PI double staining, respectively. The mitochondrial membrane potential (MMP) of differentiated PC12 cells was analyzed by JC-1 staining. The expression levels of proteins were detected by western blot analysis. We found that AA significantly increased the viability of differentiated PC12 cells but attenuated the mitochondria-mediated apoptosis dose-dependently when challenging with Aβ 25-35. Besides, the results of western blot analysis showed that AA prevented IκBα degradation and p65 nuclear translocation, and promoted the phosphorylation of Akt and GSK-3β in Aβ 25-35-treated differentiated PC12 cells. Moreover, LY294002, a specific PI3K inhibitor, was found to abolish the beneficial effects of AA on Aβ 25-35-induced apoptosis and tau protein hyperphosphorylation. Our findings demonstrated that AA protects differentiated PC12 cells from Aβ 25-35-induced apoptosis and tau protein hyperphosphorylation, which might be partially mediated by the activation of the PI3K/Akt/GSK-3β signaling pathway.
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Asiatic acid shields differentiated PC12 cells from apoptosis and tau hyperphosphorylation caused by Aβ25-35, partially mediated via activating PI3K/Akt/GSK-3β signaling.
“Cheng et al. showed that AA shields differentiated PC12 cells from apoptosis and tau protein hyperphosphorylation (pTau) caused by Aβ 25-35 , which may be partially mediated via activating the PI3K/Akt/GSK-3β signaling pathway.”
From Unlocking the Therapeutic Potential of Medicinal Plants for Alzheimer’s Disease: Preclinical to Clinical Trial Insights (2023) · cites this paper as [113]
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- Authors
- Cheng, W., Chen, W., Wang, P., & Chu, J.
- Affiliations
- Jining First People's Hospital (CN)
- Corresponding author
- Chu, Jianfeng
- Venue
- Life Sciences
- Publisher
- Elsevier BV
- Published
- 2018-09
- Volume
- 208
- Pages
- 96-101
- ISSN
- 0024-3205 (ISSN-L)
- OpenAlex
- W2827011486
- Cited by
- 57
- References
- 25
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 8 · 2023: 7 · 2022: 9 · 2021: 6 · 2020: 8 · 2019: 10
- FWCI
- 4.14
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Life Sciences (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Complementary and alternative medicine › Medicinal Plants and Neuroprotection
- Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
- Keywords
- asiatic acid, amyloid beta 25-35, neurotoxicity, apoptosis, tau hyperphosphorylation, PI3K/Akt/GSK-3β signaling, Alzheimer's disease, PC12 cells, mitochondrial membrane potential, NF-κB, neuroprotection
- MeSH terms
- Glycogen Synthase Kinase 3 beta, Animals, Cell Differentiation, Peptide Fragments, Phosphorylation, Signal Transduction, Amyloid beta-Peptides, PC12 Cells, Apoptosis, Neuroprotective Agents, Phosphatidylinositol 3-Kinases, Proto-Oncogene Proteins c-akt, Rats, Membrane Potential, Mitochondrial, Pentacyclic Triterpenes
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