Background The high-mobility group box 1 (HMGB1)/receptor for advanced glycation end products (RAGE) signaling pathway holds promise as a potential therapeutic target for ischemic brain injury. The effects of FPS-ZM1 and electroacupuncture (EA) on activation of the HMGB1/RAGE signaling pathway after cerebral ischemia remain uncertain. Methods Middle cerebral artery occlusion (MCAO) model was established. Neurological function was assessed using Longa scores. Nissl staining was used to observe the morphology of neurons. The expression levels of HMGB1 and RAGE were assayed with immunofluorescence staining and western blot. Results The results showed that EA and FPS-ZM1 could reduce the neural function score and neurons cell injury in cerebral ischemia rats by inhibiting the expression of HMGB1 and RAGE in primary motor cortex (M1) region. In addition, EA combined with FPS-ZM1 had a better therapeutic effect. Conclusions The HMGB1/RAGE pathway could be activated after cerebral ischemia. Both EA and FPS-ZM1 improved neurological deficits and attenuated neuronal damage in rats. They had synergistic effects. These interventions were observed to mitigate brain damage by suppressing the activation of HMGB1/RAGE.

中文翻译：

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电针抑制HMGB1/RAGE的表达，减轻脑缺血大鼠初级运动皮层损伤。

背景 高迁移率族盒 1 (HMGB1)/晚期糖基化终末产物受体 (RAGE) 信号通路有望成为缺血性脑损伤的潜在治疗靶点。FPS-ZM1 和电针 (EA) 对脑缺血后 HMGB1/RAGE 信号通路激活的影响仍不确定。方法建立大脑中动脉闭塞（MCAO）模型。使用 Longa 评分评估神经功能。采用尼氏染色观察神经元形态。采用免疫荧光染色和western blot检测HMGB1和RAGE的表达水平。结果结果显示，EA和FPS-ZM1可通过抑制初级运动皮层（M1）区HMGB1和RAGE的表达，减轻脑缺血大鼠的神经功能评分和神经元细胞损伤。此外，EA联合FPS-ZM1有更好的治疗效果。结论 脑缺血后HMGB1/RAGE通路可能被激活。EA 和 FPS-ZM1 均可改善大鼠的神经功能缺陷并减轻神经元损伤。它们具有协同效应。研究发现这些干预措施通过抑制 HMGB1/RAGE 的激活来减轻脑损伤。