Wu Chunxiao, Wang Jiao, Li Chun, Zhou Guoping, Xu Xiuhong, Zhang Xin, Lan Xiao
School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong Province 510515, China.
College of Acupuncture, Moxibustion, and Tuina, Hunan University of Chinese Medicine, Changsha, Hunan 410007, China.
Evid Based Complement Alternat Med. 2015;2015:414965. doi: 10.1155/2015/414965. Epub 2015 Nov 8.
Background. EA therapy is a traditional therapeutic approach for alleviation of cerebral I/R-induced brain injury. We investigated the effect of EA on MCAO rat model to examine the mechanism of apoptosis in the rat hippocampus. Methods. 200 male Sprague-Dawley rats were randomly divided into sham, I/R, EA, ERK inhibitor (PD), and ERK inhibitor+EA (PD+EA) groups. Each group was subdivided into 5 groups according to different time points. Locomotor behaviors were evaluated using neurological scales and morphological examination was performed using HE staining. Apoptosis index of neural cells in local infarcted area was measured by TUNEL and p-ERK expression was detected using immunohistochemistry technique and western blot analysis. Results. Neurological deficit scores and neural apoptosis in the EA group were lower than I/R group at the same time points, respectively. At different time points, p-ERK level was increased in the ischemic hippocampal CA1 in the EA group as compared to I/R group; the increased level was increased most at 1 day, 3 days, and 1 week (p < 0.01). Conclusion. EA alleviates neurological deficit, reduces apoptosis index, and simultaneously upregulates the expression of p-ERK signal pathway in rats subjected to I/R injury.
背景。电针疗法是缓解脑缺血/再灌注(I/R)诱导的脑损伤的一种传统治疗方法。我们研究了电针对大脑中动脉闭塞(MCAO)大鼠模型的影响,以探讨大鼠海马体中细胞凋亡的机制。方法。将200只雄性Sprague-Dawley大鼠随机分为假手术组、I/R组、电针组、ERK抑制剂(PD)组和ERK抑制剂+电针(PD+EA)组。根据不同时间点,每组再细分为5个小组。使用神经学量表评估运动行为,并使用苏木精-伊红(HE)染色进行形态学检查。通过末端脱氧核苷酸转移酶介导的缺口末端标记法(TUNEL)测量局部梗死区域神经细胞的凋亡指数,并使用免疫组织化学技术和蛋白质免疫印迹分析检测p-ERK表达。结果。在相同时间点,电针组的神经功能缺损评分和神经细胞凋亡分别低于I/R组。在不同时间点,与I/R组相比,电针组缺血海马CA1区的p-ERK水平升高;在第1天、第3天和第1周升高最为明显(p<0.01)。结论。电针可减轻神经功能缺损,降低凋亡指数,并同时上调I/R损伤大鼠p-ERK信号通路的表达。