Wu Chunxiao, Li Chun, Zhou Guoping, Yang Lu, Jiang Guimei, Chen Jing, Li Qiushi, Zhan Zhulian, Xu Xiuhong, Zhang Xin
School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong Province, China.
School of Acupuncture & Moxibustion and Tui-na, Hunan University of Chinese Medicine, Changsha, Hunan Province, China.
Acupunct Med. 2017 Dec;35(6):430-436. doi: 10.1136/acupmed-2016-011121. Epub 2017 Jun 17.
To explore the effects of electroacupuncture (EA) on the phosphorylated extracellular signal regulated kinase (p-ERK) pathway of the cerebral cortex in a rat model of focal cerebral ischaemia/reperfusion (I/R).
160 adult Sprague-Dawley rats underwent middle carotid artery occlusion (MCAO) to establish I/R injury and were randomly divided into four groups (n=40 each) that remained untreated (I/R group) or received EA at LU5, LI4, ST36 and SP6 (I/R+EA group), the ERK inhibitor PD98059 (I/R+PD group), or both interventions (I/R+PD+EA groups). An additional 40 rats undergoing sham surgery formed a healthy control group. Eight rats from each group were sacrificed at the following time points: 2 hours, 6 hours, 1 day, 3 days and 1 week. Neurological function was assessed using neurological deficit scores, morphological examination was performed following haematoxylin-eosin staining of cortical tissues, and apoptotic indices were calculated after terminal deoxyribonucleotidyl transferase (TdT)-mediated biotin-16-dUTP nick-end labelling. Cortical protein and mRNA expression of p-ERK and ERK were measured by immunohistochemistry and real-time quantitative PCR, respectively.
Compared with the I/R group, neurological deficit scores and apoptotic indices were lower in the I/R+EA group at 1 and 3 days, whereas mRNA/protein expression of ERK/p-ERK was higher in the EA group at all time points studied.
Our results suggest that EA can alleviate neurological deficits and reduce cortical apoptosis in rats with I/R injury. These anti-apoptotic effects may be due to upregulation of p-ERK. Moreover, apoptosis appeared to peak at 1 day after I/R injury, which might therefore represent the optimal time point for targeting of EA.
探讨电针（EA）对局灶性脑缺血/再灌注（I/R）大鼠模型大脑皮质磷酸化细胞外信号调节激酶（p-ERK）通路的影响。
160只成年Sprague-Dawley大鼠行大脑中动脉闭塞（MCAO）以建立I/R损伤模型，并随机分为四组（每组n = 40只），分别为不接受任何治疗（I/R组）、在肺经5穴、大肠经4穴、胃经36穴和脾经6穴接受电针治疗（I/R + EA组）、给予ERK抑制剂PD98059（I/R + PD组）或两种干预措施联合使用（I/R + PD + EA组）。另外40只接受假手术的大鼠作为健康对照组。每组8只大鼠在以下时间点处死：2小时、6小时、1天、3天和1周。采用神经功能缺损评分评估神经功能，对皮质组织进行苏木精-伊红染色后进行形态学检查，并在末端脱氧核苷酸转移酶（TdT）介导的生物素-16-dUTP缺口末端标记后计算凋亡指数。分别通过免疫组织化学和实时定量PCR检测皮质中p-ERK和ERK的蛋白及mRNA表达。
与I/R组相比，I/R + EA组在1天和3天时神经功能缺损评分及凋亡指数较低，而在所有研究时间点，EA组ERK/p-ERK的mRNA/蛋白表达均较高。
我们的结果表明，电针可减轻I/R损伤大鼠的神经功能缺损并减少皮质细胞凋亡。这些抗凋亡作用可能归因于p-ERK的上调。此外，凋亡似乎在I/R损伤后1天达到峰值，因此这可能是电针治疗的最佳时间点。
