Acupoint catgut embedding alleviates experimental autoimmune encephalomyelitis by modulating neuroinflammation and potentially inhibiting glia activation through JNK and ERK pathways.

Researchers investigated whether acupoint catgut embedding (ACE)—a traditional Chinese medicine technique where dissolvable surgical thread is implanted at acupuncture points—could help treat neuroinflammation using an animal model of autoimmune disease. ACE is already used for chronic pain and allergic conditions, but scientists wanted to understand how it affects the nervous system and immune response. In this study, mice with experimental autoimmune encephalomyelitis (EAE), which mimics human autoimmune brain inflammation, received ACE treatment at specific acupuncture points. The results showed significant improvements: treated mice had less severe disease symptoms, reduced anxiety-like behaviors, and decreased inflammation and nerve damage in their spinal cords. The treatment worked by rebalancing the immune system—reducing harmful inflammatory immune cells (Th17 and Th1) while increasing protective regulatory cells (Tregs). Blood tests confirmed lower levels of inflammatory chemicals. Importantly, researchers discovered that ACE calmed overactive brain support cells called microglia and astrocytes, which normally contribute to inflammation during autoimmune conditions. These effects appeared to work through specific molecular pathways (JNK and ERK signaling). While this study used an animal model and more research is needed in humans, the findings suggest ACE may help manage neuroinflammatory conditions by addressing both immune dysfunction and brain inflammation simultaneously. The technique's ability to provide sustained stimulation at acupuncture points over time may offer advantages for chronic inflammatory conditions. Anyone considering ACE should consult a licensed acupuncturist or traditional Chinese medicine practitioner trained in this specialized technique.

This study examined acupoint catgut embedding (ACE) efficacy in experimental autoimmune encephalomyelitis (EAE) mice, an established model for autoimmune neuroinflammation. ACE treatment significantly reduced EAE severity scores and anxiety-like behaviors while decreasing spinal cord inflammation and demyelination. Immunological analysis via flow cytometry and ELISA demonstrated restored immune homeostasis with decreased Th17 and Th1 cells, elevated Treg populations in peripheral lymphoid organs, and reduced serum inflammatory cytokine levels. RNA sequencing of spinal cord tissue revealed downregulation of genes associated with reactive gliosis. Immunofluorescence confirmed suppressed microglial and astrocytic activation. Western blotting and qRT-PCR validated that ACE inhibited ERK and JNK signaling pathways at transcriptional and protein levels. The study suggests ACE exerts neuroprotective effects through dual mechanisms: peripheral immune modulation and central nervous system glial regulation. These findings provide mechanistic evidence supporting ACE as a potential therapeutic intervention for neuroinflammatory conditions, warranting translation to clinical investigation in autoimmune neurological disorders.