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Neuroprotective mechanism of Ribisin A on Aβ25-35-induced PC12 cell damage model
Xinyue Du1, Mengyu Bao1, Yuanyuan Li1
1School of Pharmaceutical Sciences, Shandong Key Laboratory of Digital Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan 250355, China.
Tissue & Cell
|July 31, 2026
Summary
Ribisin A demonstrates neuroprotective effects against amyloid-β (Aβ) induced damage in Alzheimer
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Amyloid-β (Aβ) deposition is a hallmark of Alzheimer's disease (AD).
- Ribisin A, a benzofuran compound from Phellinus ribis, exhibits potential neuroprotective properties.
- Understanding Ribisin A's mechanism is crucial for AD therapeutic development.
Purpose of the Study:
- To investigate the neuroprotective mechanism of Ribisin A in an in vitro Alzheimer's disease model.
- To elucidate Ribisin A's effects on Aβ₂₅₋₃₅-induced neuronal damage and the ERK pathway.
Main Methods:
- Established an in vitro AD model using PC12 cells exposed to Aβ₂₅₋₃₅.
- Utilized MTT assays, ELISA, flow cytometry, and western blotting to assess cellular damage, cytokine levels, Ca²⁺ concentration, mitochondrial membrane potential (MMP), and ERK pathway proteins.
- Analyzed the expression of TrkB, p-ERK1/2, and p-CREB.
Main Results:
- Ribisin A reduced markers of cellular injury including LDH, ROS, TNF-α, and IL-6, while increasing SOD.
- It normalized Ca²⁺ levels and MMP, mitigating Aβ₂₅₋₃₅-induced mitochondrial dysfunction.
- Ribisin A upregulated TrkB, p-ERK1/2, and p-CREB, enhancing ERK/CREB signaling.
Conclusions:
- Ribisin A exerts neuroprotection by reducing oxidative stress, inflammation, and apoptosis.
- Its mechanism involves the TrkB-mediated ERK/CREB signaling cascade.
- Ribisin A shows promise as a therapeutic agent for Alzheimer's disease.
