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Updated: Mar 9, 2026
Identifying Microglia and Peripheral Infiltrating Macrophages in the Injured Spinal Cords Using Flow Cytometry
Published on: June 24, 2025
Electroacupuncture alleviates the inflammatory response via effects on M1 and M2 macrophages after spinal cord injury
Jiagui Zhao1, Likui Wang1, Yuanhai Li1
1Department of Anesthesiology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui Province, China.
Background:
Macrophages/microglia are important effector cells at the site of spinal cord injury (SCI). M1-type macrophages facilitate innate immunity to remove foreign microbes and wound debris from the injury site. M2-type macrophages exhibit tissue repair properties and attenuate production of pro-inflammatory cytokines. Regulation of the polarisation of M1/M2 macrophages may affect the inflammatory response in SCI and may be related to neurotrophin-3 (NT-3). Electroacupuncture (EA) at GV acupuncture points can be used as an adjuvant therapy for SCI.
Aim:
To investigate the effects of EA on Basso, Beattie and Bresnahan (BBB) functional evaluation and inflammatory cytokines (tumour necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and IL-10), and on the proportions of M1/M2 macrophages, and to provide a greater understanding of the mechanisms underlying the potential clinical treatment of SCI.
Methods:
A rat SCI model was induced by spinal segment transection at T10 in 16 Sprague-Dawley rats. A further eight rats were included as a Control group. Ten surviving SCI model rats were divided into two groups (n=5 each): an SCI group that remained untreated; and an SCI+EA group that received EA at GV6 and GV9.
Results:
EA improved BBB scores, inhibited the proportion of M1 macrophages and TNF-α, IL-1β and IL-6 levels, and downregulated the M1 marker CD86. By contrast, EA enhanced IL-10, the proportion of M2 macrophages and upregulated the M2 marker CD206 and NT-3 expression.
Conclusions:
EA had a positive impact on SCI model rats. This may be related to the neuroprotective effect of NT-3, which may increase the polarisation of M2 microglia/macrophages.
Insights
Electroacupuncture (EA) improves spinal cord injury (SCI) outcomes by shifting macrophage polarization from M1 to M2. This neuroprotective effect, potentially mediated by neurotrophin-3 (NT-3), reduces inflammation and promotes tissue repair.
Area of Science:
- Neuroscience
- Immunology
- Regenerative Medicine
Background:
- Macrophages and microglia are key players in spinal cord injury (SCI) response, with M1 types promoting inflammation and M2 types aiding tissue repair.
- The balance of M1/M2 macrophage polarization influences SCI outcomes and may involve neurotrophin-3 (NT-3).
- Electroacupuncture (EA) is explored as an adjuvant therapy for SCI.
Purpose of the Study:
- To evaluate the impact of EA on functional recovery (BBB scores) in a rat SCI model.
- To assess EA's effects on inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-10) and M1/M2 macrophage proportions.
- To elucidate the underlying mechanisms of EA's potential therapeutic benefits in SCI.
Main Methods:
- A T10 spinal cord transection model was established in Sprague-Dawley rats.
- Surviving SCI rats were divided into untreated SCI and EA-treated groups (EA applied at GV6 and GV9).
- Functional recovery (BBB scores), cytokine levels, and M1/M2 macrophage markers (CD86, CD206) were analyzed.
Main Results:
- EA treatment significantly improved BBB functional scores in SCI rats.
- EA inhibited M1 macrophage proportion, downregulated M1 marker CD86, and reduced pro-inflammatory cytokines (TNF-α, IL-1β, IL-6).
- EA enhanced M2 macrophage proportion, upregulated M2 marker CD206, increased anti-inflammatory cytokine IL-10, and boosted NT-3 expression.
Conclusions:
- EA demonstrates a positive therapeutic effect in a rat model of spinal cord injury.
- EA promotes a shift towards M2 macrophage polarization, reducing inflammation and potentially enhancing tissue repair.
- The neuroprotective role of NT-3 may be involved in EA's mechanism, promoting M2 microglia/macrophage polarization.
