Li Jing, He Jiaojun, Du Yuanhao, Cui Jingjun, Ma Ying, Zhang Xuezhu
Department of Acupuncture and Moxibustion Research Institute, First Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China.
BMC Complement Altern Med. 2014 Nov 11;14:441. doi: 10.1186/1472-6882-14-441.
To investigate the effects and potential mechanism of electroacupuncture intervention on expressions of Angiotensin II and its receptors-mediated signaling pathway in experimentally induced cerebral ischemia.
Totally 126 male Wistar rats were randomly divided into control group, model group and EA group. The latter two were further divided into ten subgroups (n = 6) following Middle Cerebral Artery Occlusion (MCAO). Changes in regional cerebral blood flow (rCBF) and expressions of Angiotensin II and its receptors (AT1R, AT2R), as well as effector proteins in phosphatidyl inositol signal pathway were monitored before and at different times after MCAO.
MCAO-induced decline of ipsilateral rCBF was partially suppressed by electroacupuncture, and contralateral blood flow was also superior to that of model group. Angiotensin II level was remarkably elevated immediately after MCAO, while electroacupuncture group exhibited significantly lower levels at 1 to 3 h and the value was significantly increased thereafter. The enhanced expression of AT1R was partially inhibited by electroacupuncture, while increased AT2R level was further induced. Electroacupuncture stimulation attenuated and postponed the upregulated-expressions of Gq and CaM these upregulations. ELISA results showed sharply increased expressions of DAG and IP3, which were remarkably neutralized by electroacupuncture.
MCAO induced significant increases in expression of Angiotensin II and its receptor-mediated signal pathway. These enhanced expressions were significantly attenuated by electroacupuncture intervention, followed by reduced vasoconstriction and improved blood supply in ischemic region, and ultimately conferred beneficial effects on cerebral ischemia.
探讨电针干预对实验性脑缺血中血管紧张素II及其受体介导信号通路表达的影响及潜在机制。
将126只雄性Wistar大鼠随机分为对照组、模型组和电针组。后两组在大脑中动脉闭塞(MCAO)后进一步分为10个亚组(n = 6)。在MCAO前及MCAO后不同时间监测局部脑血流量(rCBF)变化、血管紧张素II及其受体(AT1R、AT2R)的表达,以及磷脂酰肌醇信号通路中的效应蛋白。
电针部分抑制了MCAO诱导的同侧rCBF下降,对侧血流量也优于模型组。MCAO后即刻血管紧张素II水平显著升高,而电针组在1至3小时时水平显著降低,此后该值显著升高。电针部分抑制了AT1R表达的增强,同时进一步诱导了AT2R水平的升高。电针刺激减弱并推迟了Gq和CaM的上调表达。ELISA结果显示二酰甘油(DAG)和肌醇三磷酸(IP3)的表达急剧增加,电针显著中和了这些增加。
MCAO诱导血管紧张素II及其受体介导的信号通路表达显著增加。电针干预显著减弱了这些增强的表达,随后减少了血管收缩,改善了缺血区域的血液供应,最终对脑缺血产生有益影响。