Effects of electroacupuncture at points selected by orthogonal experiment on the extracellular signal regulated kinase signal pathway in a rat model of cerebral ischenia-reperfusion injury
10.3969/j.issn.2095-4344.2016.40.004
- VernacularTitle:正交法筛选组穴对脑缺血再灌注损伤模型大鼠细胞外信号调节激酶信号转导通路的影响
- Author:
Yihui FENG
;
Zhihua ZHU
;
Chunxiao WU
;
Guoping ZHOU
- Publication Type:Journal Article
- Keywords:
Electroacupuncture;
Brain Ischemia;
Tissue Engineering
- From:
Chinese Journal of Tissue Engineering Research
2016;20(40):5953-5958
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:Acupuncture point matching is little reported in the electroacupuncture for cerebral ischemia-reperfusion injury.
OBJECTIVE:To explore the influence of electroacupuncture acupoints selected by orthogonal experiment on rats with cerebral ischemia reperfusion and extracel ular signal regulated kinase (ERK) signal pathway.
METHODS:150 Sprague-Dawley rats were randomly divided into five groups:sham operation group rats were exposed the middle cerebral artery only;models of cerebral ischemia reperfusion were established in the rats in model and orthogonal groups. Then rats in the orthogonal groups 1 (Baihui (DU 20), Quchi (LI 11), Zusanli (ST 36), and Chize (LU 5)), 2 (Baihui (DU 20), Zusanli (ST 36), Chize (LU 5), and Sanyinjiao (SP 6)) and 3 (Hegu (LI 4), Zusanli (ST 36), Chize (LU 5) and Sanyinjiao (SP 6)) were given electroacupuncture at acupoints selected by orthogonal experiment, respectively.
RESULTS AND CONCLUSION:Compared with the model group, in al orthogonal groups, the neurological function deficit scores were decreased, infarct volume was smal er, the number of microvessel density in the ischemia region and the p-ERK expression level in the cortex and hippocampal CA1 region of ischemic hemisphere were increased, and significant changes were found in the orthogonal group 3. These findings indicate that electroacupuncture at points of Hegu (LI 4), Zusanli (ST 36), Chize (LU 5) and Sanyinjiao (SP 6) selected by orthogonal experiment can significantly reduce the infarct volume of cerebral ischemia-reperfusion injury in rats possibly by regulating the ERK signaling pathway.
