Yuan et al. (2026)
- Authors: Yi-Na Yuan, Di Liu, Jun-Wei Liu, Long Li, Yong-Li Wu, Hua-Yuan Li
- Institutes: Department of Traditional Chinese Medicine, Ningxia Medical University, Yinchuan, China
- Publisher: Zhen Ci Yan Jiu (Acupuncture Research)
- Link: DOI
Summary
This study identifies a specific biological pathway through which warming needle moxibustion may alleviate fatigue symptoms. By demonstrating that this traditional therapy can repair mitochondrial function in skeletal muscle, the research provides a modern scientific framework for why moxibustion might benefit individuals with Chronic Fatigue Syndrome.
What was researched?
The study investigated how warming needle moxibustion (WNM) affects mitochondrial health and the AMPK/ULK1 signaling pathway in the skeletal muscle of rats with chronic fatigue syndrome.
Why was it researched?
Researchers aimed to explore the underlying biological mechanisms of WNM, specifically focusing on whether it can improve fatigue by regulating mitochondrial autophagy and energy metabolism.
How was it researched?
Male rats were divided into control, CFS model, WNM, and coenzyme Q10 💊 groups. The WNM group received treatment at specific acupoints (ST36, CV4, CV12) for 14 days, after which behavioral tests, mitochondrial morphology, and protein expression levels were analyzed.
What has been found?
WNM significantly increased body weight and swimming time while improving mitochondrial structure in skeletal muscle. It upregulated the expression of p-AMPK and p-ULK1, indicating that the treatment promotes mitochondrial autophagy to clear damaged components.
Discussion
The results suggest that WNM performs similarly to Coenzyme Q10 in improving CFS symptoms but specifically targets the AMPK/ULK1 pathway to restore cellular energy production. The study is limited by its animal model design, which may not perfectly replicate human ME/CFS pathophysiology.
Conclusion & Future Work
Warming needle moxibustion effectively alleviates fatigue by activating the AMPK/ULK1 signaling pathway and promoting healthy mitochondrial turnover. These findings support WNM as a viable therapeutic approach for managing CFS-related energy deficits.