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Updated: Sep 13, 2025
Assaying β-amyloid Toxicity using a Transgenic C. elegans Model
Published on: October 9, 2010
[Protective effects of escin and dextromethorphan on Alzheimer disease in Caenorhabditis elegans models]
1Department of Toxicology, Peking University School of Public Health, Key Laboratory of State Administration of Traditional Chinese Medicine for Compatibility Toxicology, Beijing Key Laboratory of Toxicological Research and Risk Assessment for Food Safety, Beijing 100191, China.
Objective:
To investigate whether escin (ESC) and dextromethorphan (DEX) have the protective effects on the progression and symptoms of Alzheimer disease (AD).
Methods:
The AD model of Caenorhabditis elegans (C. elegans) was established by transgenic amyloid β-protein (Aβ protein). Different concentrations of ESC or DEX or 50 μmol/L memantine (MEM) were used to treat the AD model worms, and their lifespan was detected. The movement ability of AD model C. elegans was evaluated by body bending frequency and head swinging frequency. The changes in cognitive functions of AD model C. elegans before and after treatment were detected by chemotaxis experiments. The changes in Aβ protein and reactive oxygen species (ROS) content in C. elegans were detected. The changes in gene pathways related to oxidative stress were detected by Real-time quantitative polymerase chain reaction (RT-qPCR).
Results:
At high dose 1 000 μmol/L, ESC or DEX treatment showed no significant effects on the activity of C. elegans. Compared with untreated worms, the survival time of AD model C. elegans in the 20 μmol/L ESC and 60 μmol/L DEX intervention groups was significantly extended. In the middle stage of AD progression, the body bending frequency and head swinging frequency of AD model worms after ESC or DEX treatment was significantly increased compared with the untreated control group with DEX being more effective in the recovery of head swinging frequency. For the early cognitive function tests, the chemotaxis index of ESC or DEX treated worms was significantly higher than that of the untreated worms, which correlated with marked reductions in the Aβ protein levels. The reactive oxygen species content in the drug intervention group was also lower than that in the control group. RT-qPCR results showed that ESC could inhibit oxidative stress in the AD model C. elegans by a 2-fold upregulation of skn1 expression.
Conclusion:
ESC and DEX could improve the reductions of movement ability and cognitive function in the AD model worms and delay the aggravation of AD-related symptoms. ESC delays the progression of AD possibly by activating the SKN-1/Nrf2 pathway to protect against oxidative injury in the AD model.
