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Objective: To systematically evaluate the effects of various complementary and alternative medicine (CAM) non-pharmacological therapies on fatigue levels, oxidative stress, inflammation, and endocrine indicators in chronic fatigue-like conditions animal models, and to rank the efficacy of these interventions. Methods: A computerized search was conducted across databases including PubMed, Cochrane Library, Embase, Web of Science, CNKI, Wanfang, VIP, and CBMdisc, to collect animal experiments on fatigue-like conditions treated with CAM non-pharmacological therapies published from the establishment of the databases to January 14, 2026. Two researchers independently screened the literature, extracted data, and assessed risk of bias. Stata 16.0 software was used for network meta-analysis, and SYRCLE's risk of bias tool was employed to evaluate the quality of the included studies. Results: A total of 77 studies involving nine types of CAM non-pharmacological therapies were included. In terms of improving fatigue levels, compared to the control group, electroacupuncture (MD = 347.00 s, 95% CI 144.70, 549.29) and moxibustion (MD = 311.28 s, 95% CI 146.36, 476.20) significantly prolonged exhaustive swimming time. In terms of improving oxidative stress damage, fire acupuncture (MD = -13.15 nmol/ml, 95% CI -18.06, -8.24), manual acupuncture (MD = -3.85 nmol/ml, 95% CI -5.12, -2.58), needle-pricking (MD = -11.43 nmol/ml, 95% CI -16.54, -6.32), and moxibustion (MD = -479.16 nmol/ml, 95% CI -567.05, -391.27) significantly reduced MDA levels. In terms of improving inflammatory damage, Tuina (MD = -552.03 pg/ml, 95% CI -700.81, -403.25) and electroacupuncture (MD = -156.59 pg/ml, 95% CI -259.85, -53.34) can significantly reduce the level of IL-1β. In terms of regulating endocrine, electroacupuncture (MD = -9.91 pg/ml, 95% CI -14.77, -5.05) and Tuina (MD = -16.96 pg/ml, 95% CI -25.37, -8.55) can significantly reduce the level of CRH. Conclusion: Non-pharmacological therapies in complementary and alternative medicine have great potential in improving fatigue-related phenotypes, oxidative stress damage, inflammatory damage, and regulating endocrine levels in animal models of fatigue-like conditions. Future research should focus on developing animal models that better replicate the pathogenesis and core characteristics of CFS, and then extend them to randomized controlled trials involving CFS patients to verify the transformation potential. Systematic review registration: https://www.crd.york.ac.uk/prospero/, identifier CRD420251177070.
Ren et al. (Thu,) studied this question.