World Journal of Acupuncture - Moxibustion · Published 2026-02-27 · DOI 10.1016/j.wjam.2026.02.001
Objective: Cerebrovascular repair plays a crucial role in promoting post-stroke neurological recovery. However, effective strategies to enhance cerebrovascular repair and the underlying mechanisms remain elusive. Here, we investigated whether post-stroke electroacupuncture (EA) treatment could promote cerebrovascular repair and thereby improve neurological function, as well as the potential mechanisms involved. Methods: Eight-week-old male C57BL/6 J mice were subjected to photothrombosis-induced brain ischemia. Following successful model induction, the mice were randomly assigned to the model group, the EA continuous wave group (EA[Co]), and the EA dense-sparse wave group (EA[SD]), with 10 animals in each group. A sham-operated group (n = 10) served as the control. The EA groups received a 4-week EA intervention targeting the acupoints “Neiguan(PC6)” and “Sanyinjiao(SP6)”. EA was administered five times per week with bilateral stimulation, and the affected side was connected to the EA device. The EA(SD) group received stimulation at 2/10 Hz, whereas the EA(Co) group received continuous wave stimulation at 2 Hz or 50 Hz; both were delivered at an intensity of 1 mA for 20 min per session. Twenty-four hours after photothrombosis induction, laser speckle contrast imaging and 2,3,5-triphenyltetrazolium chloride staining were performed to confirm model establishment and cerebral ischemic injury. Neurological function was evaluated using behavioral tests, including the adhesive removal test, hanging wire test, and elevated plus maze test. Immunofluorescence staining was performed to assess neuronal viability, cerebral microvascular structure, endothelial cell proliferation, and vascular repair markers in the peri‑infarct cortex. Results: Significant reductions in cerebral blood perfusion (P < 0.05) and non-infarct volume (P < 0.05) were observed in the ipsilateral hemisphere of model mice compared with the contralateral hemisphere, confirming successful establishment of the photothrombosis-induced ischemia model. (1) In the adhesive removal test, the model group exhibited significantly prolonged adhesive removal latency compared with the control group (P < 0.05). EA treatment shortened latency compared with the model group (P < 0.05), with no statistically significant difference between the EA(Co) and EA(SD) groups (P > 0.05). (2) In the wire hanging test, the model group exhibited significantly lower muscle strength scores than the sham group (P < 0.05). EA treatment significantly enhanced muscle strength performance (P < 0.05), and the improvement was greater in the EA(Co) group than in the EA(SD) group (P < 0.05). (3) In the elevated plus maze test, the model group showed significant decreases in total distance traveled, percentage of open-arm entries, and time spent in open arms compared with the control group (all P < 0.05). Following EA treatment, all three parameters were significantly restored compared with the model group (all P < 0.05), with no statistically significant difference between the EA(Co) and EA(SD) groups (P > 0.05). (4) Immunofluorescence staining showed a significantly reduced density of Nissl⁺/NeuN⁺ double-labeled neurons in the peri‑infarct regions of the model group compared with the control group (P < 0.05). Nissl⁺/NeuN⁺ neuronal density was significantly restored in the EA groups compared with the model group (all P < 0.05), with no statistically significant difference between the EA(Co) and EA(SD) groups (P > 0.05). (5) In terms of cerebrovascular structure, the model group exhibited significantly reduced vascular volume, microvascular branching density, and microvascular length in the peri‑infarct regions compared with the control group (all P < 0.05). EA treatment restored all three vascular parameters compared with the model group (all P < 0.05). Moreover, the EA(Co) group showed significantly greater enhancement of cerebrovascular structural integrity than the EA(SD) group (P < 0.05). (6) Compared with the control group, the model group showed no significant change in the density of Ki67⁺/CD31⁺ double-labeled endothelial cells (P > 0.05). Following EA treatment, this density was significantly increased compared with the model group (P < 0.05), with no statistically significant difference between the EA(Co) and EA(SD) groups (P > 0.05). (7) Compared with the control group, the model group exhibited significant reductions in lectin-labeled glycocalyx in vessels and basement membrane protein collagen IV expression (all P < 0.05), indicating disruption of cerebrovascular integrity. EA treatment significantly restored both indicators compared with the model group (all P < 0.05), with no statistically significant difference between the EA(Co) and EA(SD) groups (P > 0.05). Conclusion: This study demonstrates that EA promotes cerebrovascular repair and neurological recovery after ischemic stroke by enhancing microvascular remodeling, stimulating endothelial proliferation, and restoring basement membrane and glycocalyx integrity. EA(Co) is more effective than EA(SD) in repairing vascular structure. These findings provide mechanistic evidence that EA is a promising therapeutic approach for post-stroke rehabilitation and suggest that waveform optimization may enhance its clinical efficacy.
Abstract from DOAJ. Public domain (CC0 1.0).
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