Electroacupuncture Promotes Synaptic Recovery After Cerebral Ischemia-Reperfusion by Activating SIRT1 to Inhibit the
Qing Song1,2, Meng-Meng Zhao1,2, Wen-Qiang Sun1,2
1College of Acupuncture, Moxibustion and Tuina, Anhui University of Chinese Medicine, Hefei, 230012, China.
Neurochemical Research
|May 18, 2026
Summary
Electroacupuncture (EA) promotes functional recovery after cerebral ischemia-reperfusion injury (CIRI) by shifting astrocytes from a damaging A1 to a repair-supporting A2 phenotype via the SIRT1-NF-κB pathway, enhancing synaptic repair.
Area of Science:
- Neuroscience
- Neuroinflammation
- Regenerative Medicine
Background:
- Cerebral ischemia-reperfusion injury (CIRI) impairs functional recovery due to altered astrocyte phenotypes.
- Neurotoxic A1 astrocytes exacerbate damage, while A2 astrocytes support repair.
- The role of electroacupuncture (EA) in modulating astrocyte phenotypes for synaptic repair remains unclear.
Purpose of the Study:
- To investigate whether EA promotes synaptic repair in CIRI by orchestrating astrocyte phenotypic switching.
- To elucidate the underlying molecular mechanism involving the SIRT1-NF-κB axis.
Main Methods:
- Mice underwent middle cerebral artery occlusion/reperfusion (MCAO/R) and were treated with EA, SIRT1 inhibitor, or NF-κB inhibitor.
- Neurological function, cerebral blood flow, molecular markers (SIRT1, NF-κB, astrocyte markers C3 and S100A10), inflammatory cytokines, and synaptic proteins were assessed.
Main Results:
- EA significantly improved neurological function and cerebral blood flow.
- EA upregulated SIRT1 activity and suppressed NF-κB phosphorylation, promoting an anti-inflammatory shift.
- EA reduced A1 astrocyte markers (C3) and pro-inflammatory cytokines while increasing A2 markers (S100A10) and anti-inflammatory mediators.
- EA restored synaptic protein expression and ultrastructure.
Conclusions:
- EA drives astrocyte phenotypic switching from A1 to A2 via the SIRT1-NF-κB axis.
- This modulation reshapes the inflammatory microenvironment, promoting synaptic repair and functional recovery after CIRI.
