Animal study finds that moxibustion with deqi enhances cognitive function in dementia models, suggesting a new therapeutic approach.
Introduction: Research highlights blood-brain barrier (BBB) disruption as a critical factor in Alzheimer's disease (AD) progression, with proinflammatory cytokines driving this pathological process. Moxibustion, a traditional therapeutic intervention, has shown promise in improving cognitive function in dementia models; however, its effects in relation to deqi have not been fully investigated. This study aims to evaluate the efficacy of moxibustion combined with deqi in AD models. Method: Rats were randomized into normal (10), sham (10), AD model (10), and AD model with moxibustion (24) groups; the latter group was further divided, based on the tail temperature changes during moxibustion, into a non-tail temperature increase subgroup (11) and a tail temperature increase (deqi) subgroup (13). Cognitive function was then assessed using the Morris water maze test, and the integrity of the blood-brain barrier (BBB) was evaluated using Transmission electron microscopy (TEM) and Western blot analysis. Additionally, inflammatory markers involved in the process were further explored by ELISA. Result: The results demonstrated that moxibustion with deqi significantly reduced Morris water maze escape latency (P<0.01) and increased platform crossings (P<0.001) vs. AD controls. This effect was superior to non-deqi moxibustion, which only transiently reduced latency (Day 1: P<0.05; Days 2-5: NS) and showed no significant crossing improvement. Mechanistically, deqi preserved BBB integrity by upregulating laminin, occludin, and ZO-1 (all P<0.05), and downregulating VWF expression (P<0.01), while non-deqi only partially elevated ZO-1 (P<0.001). Critically, deqi suppressed hippocampal IL-1β, IL-6, TNF-α, and NF-κB (all P<0.01), whereas non-deqi reduced only IL-1β/TNF-α (P<0.05). Conclusion: This study first demonstrates that moxibustion-mediated deqi enhances cognitive recovery in AD models through dual regulation of BBB restoration and neuroinflammatory axis modulation, establishing deqi as an essential therapeutic component in moxibustion protocols.
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Lyu et al. (2026) studied this question.
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