Nie Zeyin, Miao Huachun, Li Chenyu, Wu Feng
Department of Human Anatomy, Wannan Medical College, No. 22, Wenchang West Road, Wuhu, 241002, Anhui, China.
Transl Neurosci. 2023 Oct 9;14(1):20220316. doi: 10.1515/tnsci-2022-0316. eCollection 2023 Jan 1.
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.
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.
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.
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.
高迁移率族蛋白B1（HMGB1）/晚期糖基化终产物受体（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尚不确定。
建立大脑中动脉闭塞（MCAO）模型。采用Longa评分评估神经功能。用尼氏染色观察神经元形态。用免疫荧光染色和蛋白质印迹法检测HMGB1和RAGE的表达水平。
结果表明，EA和FPS-ZM1可通过抑制初级运动皮层（M1）区HMGB1和RAGE的表达，降低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具有更好的治疗效果。
脑缺血后HMGB1/RAGE通路可被激活。EA和FPS-ZM1均可改善大鼠神经功能缺损并减轻神经元损伤。它们具有协同作用。观察到这些干预措施通过抑制HMGB1/RAGE的激活减轻脑损伤。
