Objective: To investigate the optimal timing and underlying mechanism of electroacupuncture (EA) at Baihui (GV 20) and Dazhui (GV 14) for improved long-term functional recovery after focal cerebral ischemia in a photothrombotic stroke mouse model.
Methods: Totally 50 adult male C57BL/6J mice were assigned into 5 groups: (a) the control group, sham-operated mice (n = 10); (b) the vehicle group, focal cerebral ischemia induction without EA (n = 10); (c) the acute EA group, mice received EA immediately post-ischemia, followed by once-daily treatments for 7 consecutive days (n = 10); (d) the subacute EA group, mice received EA 4 days post-ischemia, followed by once-daily treatments for 7 consecutive days (n = 10); (e) the delayed EA group. EA stimulation (2 Hz, 2 V for 20 min) was applied to acupuncture points (acupoints), Baihui (GV 20) and Dazhui (GV 14), once a day for 7 consecutive days beginning immediately (acute treatment), 4 d (subacute treatment) and 10 d (delayed treatment) after focal cerebral ischemia in C57BL/6J mice. Behavioral assessments were conducted 21 and 28 d post-ischemia and histopathological analyses were performed 28 days post-ischemia.
Results: The subacute EA treatment at Baihui (GV 20) and Dazhui (GV 14) significantly improved functional recovery compared to the vehicle group 28 d after ischemic brain injury, although brain atrophy was not reduced. The number of NeuN+ and NeuN+/BrdU+ cells as well as GFAP intensity in the ipsilateral cortex were significantly increased in the subacute group compared to the vehicle group 28 d post-ischemia. We concluded that EA stimulation 4 d post-ischemia (subacute treatment) enhanced neurogenesis and astrogliosis, likely contributing to long-term functional recovery following focal cerebral ischemia.
Conclusion: Our findings suggest that the timing of the EA therapy at Baihui (GV 20) and Dazhui (GV 14) determines the therapeutic effects in mice with focal cerebral ischemia induced by photothrombotic occlusion.
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Article Synopsis
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- * Results showed that sleep-deprived rats had impaired learning and memory linked to decreased synaptic density and protein expression, but EA treatment significantly improved these outcomes by enhancing synaptic structure and increasing the levels of PSD95 and MeCP
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