Astragalus polysaccharide ameliorated complex factor-induced chronic fatigue syndrome by modulating the gut microbiota and metabolites in mice. — CFSMEATLAS
Astragalus polysaccharide ameliorated complex factor-induced chronic fatigue syndrome by modulating the gut microbiota and metabolites in mice.
Wei, Xintong, Xin, Jiayun, Chen, Wei et al. · Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023 · DOI
Quick Summary
This study tested whether astragalus polysaccharide (APS), a compound from traditional Chinese medicine, could help with chronic fatigue syndrome in mice. The researchers found that APS improved fatigue-related symptoms by changing the bacteria in the gut, which led to more production of beneficial compounds called short-chain fatty acids that reduced inflammation and oxidative stress in the brain.
Why It Matters
This study provides mechanistic insight into how gut microbiota alterations and reduced SCFA production may contribute to ME/CFS pathophysiology, and identifies a potential therapeutic approach. Understanding the gut-brain axis connection in fatigue syndromes could inform future human clinical trials of microbiota-modulating interventions.
Observed Findings
APS treatment increased the abundance of short-chain fatty acid-producing bacteria in the gut microbiota.
APS restored reduced levels of short-chain fatty acids (particularly butyrate) in cecal content.
APS reversed abnormal expression of Nrf2 and NF-κB signaling pathways in the brain-gut axis.
Butyrate demonstrated antioxidant and anti-inflammatory effects when applied to neuronal cells in culture.
APS improved behavioral and fatigue-related measures in the CFS mouse model.
Inferred Conclusions
APS ameliorates CFS symptoms by modulating the composition of gut microbiota and increasing SCFA production.
SCFAs, particularly butyrate, can reduce oxidative stress and inflammation in the brain through effects on the brain-gut axis.
The Nrf2/NF-κB signaling pathway may be a key mechanism linking microbiota dysbiosis to neuroinflammation in CFS.
Remaining Questions
Do these findings translate to human ME/CFS patients, and what would be the appropriate dose and duration of APS treatment?
Are the beneficial effects of APS dependent solely on SCFA production, or are other microbial metabolites involved?
What This Study Does Not Prove
This study does not demonstrate that APS is effective in humans with ME/CFS; it is a mouse model study. It does not prove that altered gut microbiota causes ME/CFS (correlation vs. causation), nor does it establish that SCFA supplementation alone would replicate these benefits in humans. The findings may not translate to human patients due to differences in disease pathophysiology, microbiota composition, and metabolism.