Acetyl-L-carnitine attenuates Poly I:C-induced sickness behavior in mice
Suzuka Miura1, Eri Oyanagi1, Chihiro Watanabe1
1Department of Health and Sports Science.
Bioscience, Biotechnology, and Biochemistry
|August 9, 2022
Summary
Acetyl-L-carnitine (ALC) prevents Poly I:C-induced fatigue and malaise in mice. ALC enhances brain-derived neurotrophic factor (BDNF) and translocator protein (TSPO) expression, promoting quicker recovery from sickness behavior.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Fatigue and malaise are common symptoms associated with decreased physical activity.
- Acetyl-L-carnitine (ALC) is a compound that may alleviate fatigue.
- Polyriboinosinic:polyribovitics (Poly I:C) can induce sickness behavior, mimicking fatigue-like symptoms.
Purpose of the Study:
- To investigate the preventive effects of acetyl-L-carnitine (ALC) on Poly I:C-induced sickness behavior in mice.
- To understand the molecular mechanisms underlying ALC's potential protective effects.
Main Methods:
- Male C3H/HeN mice were pre-treated with ALC for 5 days.
- Poly I:C was administered to induce sickness behavior.
- Wheel running activity was monitored to assess physical activity levels.
- Gene expression of brain-derived neurotrophic factor (BDNF) and translocator protein 18kDa (TSPO) was analyzed in the cerebrum and hippocampus.
Main Results:
- ALC administration significantly attenuated the decrease in wheel running activity 24 hours post-Poly I:C.
- ALC-treated mice exhibited a faster recovery from Poly I:C-induced sickness behavior.
- Gene expression of BDNF and TSPO was higher in the ALC-treated group compared to controls.
- Upregulation of TSPO suggests enhanced cytoprotective effects in the brain.
Conclusions:
- ALC demonstrates preventive effects against Poly I:C-induced sickness behavior in mice.
- ALC may exert its beneficial effects by enhancing BDNF and TSPO expression in the brain.
- These findings suggest ALC could be a potential therapeutic agent for fatigue-related conditions.


