Electroacupuncture reduces cerebral ischemia-induced neuronal damage in the hippocampal CA1 region in rats by inhibiting HMGB1 and p-JNK overexpression.

IF 1.7 4区 医学 Q4 NEUROSCIENCES International Journal of Neuroscience Pub Date : 2025-02-01 Epub Date: 2023-11-30 DOI:10.1080/00207454.2023.2288541
Jian Zhao, Zeyin Nie, Huachun Miao, Feng Wu, Tongjun Ma
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Abstract

Background: 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.

Objective: To elucidate the mechanism through which electroacupuncture (EA) via the Baihui (GV20) and Zusanli (ST36) acupoints protects neurons.

Methods: 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.

Results: 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.

Conclusion: EA may reduce ischemia-induced neuronal damage in the hippocampal CA1 region by inhibiting the overexpression of both HMGB1 and p-JNK.

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电针通过抑制HMGB1和p-JNK过表达减轻大鼠脑缺血诱导的海马CA1区神经元损伤。
背景:海马角氨1 (CA1)区是脑缺血后易感损伤的敏感区域。高迁移率组框1 (HMGB1)和磷酸化的c-Jun n -末端激酶(p-JNK)在脑缺血损伤的介导中发挥重要作用。目的:探讨电针经百会(GV20)和足三里(ST36)穴位对神经元的保护作用机制。方法:建立永久性大脑中动脉闭塞大鼠模型。将Sprague-Dawley大鼠分为4组:假手术组、pMCAO组、EA组和假手术组(SEA)。EA组和SEA组分别选择GV20和ST36穴进行治疗。而SEA组仅在两个穴位进行浅刺,不用电。采用神经功能缺损评分法评估神经功能,尼氏染色法检测神经元损伤。采用免疫组化染色和western blot检测HMGB1和p-JNK的表达。结果:行为学实验表明,EA治疗可改善pMCAO大鼠的神经功能缺损。尼氏染色结果显示,EA可减轻神经组织损伤。免疫组化染色和western blot结果显示,EA可抑制HMGB1和p-JNK的过表达。相比之下,SEA组没有观察到这些EA效应。结论:EA可通过抑制HMGB1和p-JNK的过表达,减轻海马CA1区缺血所致的神经元损伤。
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来源期刊
CiteScore
5.10
自引率
0.00%
发文量
132
审稿时长
2 months
期刊介绍: The International Journal of Neuroscience publishes original research articles, reviews, brief scientific reports, case studies, letters to the editor and book reviews concerned with problems of the nervous system and related clinical studies, epidemiology, neuropathology, medical and surgical treatment options and outcomes, neuropsychology and other topics related to the research and care of persons with neurologic disorders.  The focus of the journal is clinical and transitional research. Topics covered include but are not limited to: ALS, ataxia, autism, brain tumors, child neurology, demyelinating diseases, epilepsy, genetics, headache, lysosomal storage disease, mitochondrial dysfunction, movement disorders, multiple sclerosis, myopathy, neurodegenerative diseases, neuromuscular disorders, neuropharmacology, neuropsychiatry, neuropsychology, pain, sleep disorders, stroke, and other areas related to the neurosciences.
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