Related Experiment Video
Updated: Feb 28, 2026

10:09
Characterization of Immune Cell-derived Extracellular Vesicles and Studying Functional Impact on Cell Environment
Published on: June 2, 2020
7.4K
Physical activity-associated extracellular vesicles inhibit inflammagen-induced microglial activation
Chien-Yu Su1, Heng-Juei Hsu2, Tzu-Feng Wang3
1Department of Neurology, Ditmanson Medical Foundation Chia-Yi Christian Hospital, Chiayi, 600566, Taiwan.
Brain, Behavior, & Immunity - Health
|February 27, 2026
Summary
Physical activity-derived extracellular vesicles (EVs) reduce neuroinflammation by suppressing microglial activation. These EVs show potential as therapeutic agents for neurodegenerative diseases and related inflammatory conditions.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Microglial activation and neuroinflammation drive neurodegenerative diseases.
- Physical activity exhibits anti-inflammatory effects, but mechanisms are unclear.
- Exerkines, induced by exercise, modulate anti-inflammatory responses.
Purpose of the Study:
- Investigate the effects of plasma-derived extracellular vesicles (EVs) from physically active animals on microglial activation.
- Determine if EVs from treadmill-exercised rats can suppress inflammation in vitro and in vivo.
Main Methods:
- Used a rodent model of long-term treadmill-induced physical activity (TMPA).
- Administered plasma-derived EVs from TMPA-treated rats to BV2 microglia cells and LPS-treated mice.
- Tracked EV distribution in vivo using labeled EVs and assessed microglial activation.
Main Results:
- EVs from TMPA-treated rats suppressed LPS-induced inflammatory signaling in BV2 microglia.
- BV2 microglia internalized EVs within 2 hours.
- In vivo, EVs from TMPA-treated rats reduced microglial activation in the substantia nigra of LPS-treated mice.
Conclusions:
- Physical activity-derived EVs effectively suppress inflammagen-induced microglial activation.
- EVs demonstrate anti-neuroinflammatory properties.
- These findings highlight EVs as potential therapeutic agents for neuroinflammation.

