Zhao Jian, Nie Zeyin, Miao Huachun, Wu Feng, Ma Tongjun
Department of Human Anatomy, Wannan Medical College, Wuhu, China.
Int J Neurosci. 2025 Feb;135(2):132-139. doi: 10.1080/00207454.2023.2288541. Epub 2023 Nov 30.
The cornu ammonis 1 (CA1) region of the hippocampus is a sensitive area that is susceptible to injury caused by cerebral ischemia. High-mobility group box 1 (HMGB1) and phosphorylated c-Jun N-terminal kinase (p-JNK) play important roles in mediating cerebral ischemic injury.
To elucidate the mechanism through which electroacupuncture (EA) via the Baihui (GV20) and Zusanli (ST36) acupoints protects neurons.
A rat model of permanent middle cerebral artery occlusion (pMCAO) was established. Sprague-Dawley rats were divided into four groups: sham-operated control, pMCAO control, EA, and sham-EA (SEA). In the EA and SEA groups, the GV20 and ST36 acupoints were selected for treatment. However, the SEA group was treated only by superficial pricking of the skin at the two acupoints without the application of electricity. Neurological function was assessed using the neurological deficit function score, and neuronal damage was detected through Nissl staining. HMGB1 and p-JNK expression was evaluated using immunohistochemical staining and western blot assays.
The behavioural experiments showed that the EA treatment improved the neurological deficits in the pMCAO rats. The Nissl staining results revealed that EA reduced neural tissue damage. The immunohistochemical staining and western blot results showed that EA inhibited HMGB1 and p-JNK overexpression. By contrast, none of these EA effects were observed in the SEA group.
EA may reduce ischemia-induced neuronal damage in the hippocampal CA1 region by inhibiting the overexpression of both HMGB1 and p-JNK.
海马体的海马角1（CA1）区域是一个敏感区域，易受脑缺血所致损伤的影响。高迁移率族蛋白B1（HMGB1）和磷酸化c-Jun氨基末端激酶（p-JNK）在介导脑缺血损伤中发挥重要作用。
阐明通过百会（GV20）和足三里（ST36）穴位进行电针（EA）保护神经元的机制。
建立大鼠永久性大脑中动脉闭塞（pMCAO）模型。将Sprague-Dawley大鼠分为四组：假手术对照组、pMCAO对照组、EA组和假电针（SEA）组。在EA组和SEA组中，选择GV20和ST36穴位进行治疗。然而，SEA组仅通过在两个穴位处浅刺皮肤而不施加电刺激。使用神经功能缺损评分评估神经功能，并通过尼氏染色检测神经元损伤。使用免疫组织化学染色和蛋白质印迹分析评估HMGB1和p-JNK的表达。
行为学实验表明，EA治疗改善了pMCAO大鼠的神经功能缺损。尼氏染色结果显示，EA减轻了神经组织损伤。免疫组织化学染色和蛋白质印迹结果表明，EA抑制了HMGB1和p-JNK的过表达。相比之下，SEA组未观察到这些EA效应。
EA可能通过抑制HMGB1和p-JNK的过表达来减少海马CA1区缺血诱导的神经元损伤。
