Antifatigue Potential Activity of <i>Sarcodon imbricatus</i> in Acute Excise-Treated and Chronic Fatigue Syndrome in Mice via Regulation of Nrf2-Mediated Oxidative Stress.

Evidence Atlas

Antifatigue Potential Activity of Sarcodon imbricatus in Acute Excise-Treated and Chronic Fatigue Syndrome in Mice via Regulation of Nrf2-Mediated Oxidative Stress.

Wang, Xue, Qu, Yidi, Zhang, Yongfeng et al. · Oxidative medicine and cellular longevity · 2018 · DOI

Quick Summary

This study tested whether a medicinal mushroom called Sarcodon imbricatus could reduce fatigue in mice with chronic fatigue syndrome. The mushroom extract improved the mice's exercise ability, reduced tiredness, and boosted the body's natural antioxidant defenses—systems that protect cells from damage.

Why It Matters

ME/CFS pathophysiology involves mitochondrial dysfunction and oxidative stress; this study provides preclinical evidence that a natural polyphenol-rich fungus may address these core mechanisms. If validated in human trials, Sarcodon imbricatus could offer a food-based adjunct approach to managing fatigue and post-exertional malaise.

Observed Findings

Sarcodon imbricatus significantly improved exercise tolerance and reduced immobility in CFS mice across multiple fatigue models.
SI increased ATP and glycogen levels in liver and muscle while decreasing lactate and blood urea nitrogen.
SI enhanced antioxidant enzyme activity (SOD, GSH-Px) and reduced oxidative stress markers (ROS, MDA) in serum, liver, and muscle.
In CFS mice, SI upregulated expression of Nrf2 and downstream antioxidant response genes (SOD1, SOD2, HO-1, CAT).

Inferred Conclusions

Sarcodon imbricatus possesses antifatigue activity in animal models of acute and chronic fatigue.
The antifatigue effect is mediated partly through restoration of energy metabolism and activation of the Nrf2 antioxidant stress-response pathway.
Sarcodon imbricatus may warrant investigation as a natural health supplement for fatigue-related conditions.

Remaining Questions

Does Sarcodon imbricatus produce similar antifatigue and antioxidant effects in humans with ME/CFS?
What is the optimal dose and duration of treatment in human subjects, and are there adverse effects?
Which bioactive components (polyphenols, sterols, specific amino acids) are responsible for the observed effects?

What This Study Does Not Prove

This animal study does not establish efficacy, safety, or appropriate dosing in humans with ME/CFS. The mouse CFS model may not fully recapitulate human disease pathophysiology, and antioxidant benefit in mice does not guarantee clinical improvement in patients. Correlation between antioxidant markers and symptom relief does not prove causation.

Metadata

DOI: 10.1155/2018/9140896
PMID: 30050662
Review status: Machine draft
Evidence level: Early hypothesis, preprint, editorial, or weak support
Last updated: 8 April 2026

About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →

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