Electroacupuncture Promotes Synaptic Recovery After Cerebral Ischemia-Reperfusion by Activating SIRT1 to Inhibit the NF-κB Pathway and Regulate Astrocyte Phenotypic Transformation.

Researchers investigated whether electroacupuncture could help brain recovery after stroke by changing how support cells in the brain respond to injury. When blood flow is temporarily blocked and then restored to the brain—called ischemia-reperfusion injury—it triggers inflammation and damages the connections between brain cells (synapses). Support cells called astrocytes can either worsen this damage (A1 type) or help repair it (A2 type). Scientists used mice with experimentally induced stroke and treated them with electroacupuncture at two specific points on the head (GV20 and GV16) daily for seven days. They measured brain function, blood flow, inflammation markers, and synapse health. The electroacupuncture treatment significantly improved neurological function and brain blood flow compared to untreated stroke mice. Most importantly, it activated a protective protein called SIRT1, which blocked inflammatory pathways and shifted astrocytes from the harmful A1 type to the helpful A2 type. This switch reduced brain inflammation and preserved synaptic connections that are essential for brain function. When researchers blocked SIRT1 with an inhibitor drug, all the beneficial effects of electroacupuncture disappeared, proving this protein was essential for the treatment's success. For stroke patients, this research suggests electroacupuncture may enhance brain repair and functional recovery by fundamentally changing the brain's inflammatory environment and protecting neural connections. These findings add to growing evidence supporting acupuncture as a complementary therapy for stroke rehabilitation. Patients interested in acupuncture for stroke recovery should seek treatment from a licensed acupuncturist with training in neurological conditions.

This murine MCAO/R study (n=unspecified groups) investigated electroacupuncture's mechanism in post-stroke synaptic recovery. EA was applied at GV20 and GV16 daily for 7 days. Primary outcomes included neurological function, cerebral blood flow, SIRT1 activity, NF-κB phosphorylation, astrocyte phenotype markers (C3 for A1, S100A10 for A2), inflammatory cytokines, and synaptic protein expression assessed via behavioral testing, Western blot, immunofluorescence, ELISA, and TEM. EA significantly improved neurological scores and perfusion while upregulating SIRT1 protein and deacetylase activity, suppressing NF-κB phosphorylation, reducing A1 marker C3 and pro-inflammatory cytokines, and increasing A2 marker S100A10 with anti-inflammatory mediators. Synaptic protein expression and ultrastructure were restored. SIRT1 inhibitor (Selisistat) completely abolished EA benefits; NF-κB inhibitor (PDTC) replicated EA's astrocyte phenotype modulation, confirming the SIRT1→NF-κB→astrocyte phenotype axis. Clinical relevance: EA may promote stroke recovery through SIRT1-mediated astrocyte polarization toward neuroprotective phenotypes, supporting synaptic plasticity and functional restoration.