目的: 观察电针对脑缺血大鼠前扣带皮质高迁移率族蛋白1(high mobility group protein 1,HMGB1)和磷酸化的c-Jun氨基酸末端激酶(phosphorylated c-Jun N-terminal kinase,p-JNK)的表达影响,探讨电针对脑缺血大鼠前扣带皮质的保护作用及机制。方法: 将24只雄性SD大鼠随机分为假手术组、模型组、电针组和假电针组,6只/组。采用右侧大脑中动脉栓塞法制备脑缺血大鼠模型,电针组选取“百会”穴、左侧“足三里”穴进行电针刺激,1次/d,30 min/次,持续14 d;假电针组仅浅刺入两穴位皮下,接电针仪但不通电。采用Longa评分评估各组大鼠神经功能损伤情况;Nissl染色观察右侧前扣带皮质神经元的形态与分布情况;免疫组化检测右侧前扣带皮质HMGB1和p-JNK蛋白的表达情况。结果: 与假手术组相比,模型组和假电针组大鼠神经功能缺损评分升高(P＜0.01),右侧前扣带皮质区Nissl阳性神经元数量减少(P＜0.01),HMGB1和p-JNK蛋白表达增加(P＜0.01);与模型组相比,电针组大鼠在脑缺血第7天、14天时神经功能缺损评分降低(P＜0.05),Nissl阳性神经元数量增加(P＜0.01),HMGB1和p-JNK蛋白表达降低(P＜0.01)。结论: 电针可能通过抑制脑缺血后HMGB1和p-JNK的过表达,减轻前扣带皮质的损伤。
Objective: To observe the effect of electroacupuncture on the expression of high mobility group protein 1 (HMGB1) and phosphorylated c-Jun N-terminal kinase (p-JNK) in the anterior cingulate cortex of rats with cerebral ischemia, and to explore the protective effect and mechanism of electroacupuncture on the anterior cingulate cortex of rats with cerebral ischemia. Methods: Twenty-four male SD rats were randomly assigned into four groups, namely sham-operation, model, electroacupuncture, and sham-electroacupuncture groups, with 6 rats in each group. Cerebral ischemia was induced by blocking the right middle cerebral artery, creating a rat model of cerebral ischemia. Electroacupuncture was administered for 30 minutes, once daily for 14 days, targeting “Baihui”(GV20) and “Zusanli”(ST36) on the left side of the electroacupuncture group. In contrast, only the skin was penetrated in the sham-electroacupuncture group without activating the electroacupuncture device. Longa score was used to evaluate the neurological impairment of rats in each group. Nissl staining was used to observe the morphology and distribution of neurons in the right anterior cingulate cortex. The expression of HMGB1 and p-JNK protein in the right anterior cingulate cortex was detected by immunohistochemistry. Results: Compared with the sham-operation group, the neurological deficit scores of the model group and the sham-electroacupuncture group were increased (P＜0.01), the number of Nissl positive neurons in the right anterior cingulate cortex was decreased (P＜0.01), and the expression of HMGB1 and p-JNK protein was increased (P＜0.01). Compared with the model group, the neurological deficit score of the rats in the electroacupuncture group decreased on the 7th and 14th day of cerebral ischemia (P＜0.05), the number of Nissl positive neurons increased (P＜0.01), and the expression of HMGB1 and p-JNK protein decreased (P＜0.01). Conclusion: Electroacupuncture may reduce the damage of anterior cingulate cortex by inhibiting the overexpression of HMGB1 and p-JNK after cerebral ischemia.
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