Electroacupuncture promotes neurological functional recovery via the retinoic acid signaling pathway in rats following cerebral ischemia-reperfusion injury

被引:48
作者
Hong, Jiangcong [2 ,3 ]
Wu, Guangwen [2 ]
Zou, Yulong [3 ]
Tao, Jing [1 ]
Chen, Lidian
机构
[1] Fujian Univ Tradit Chinese Med, Fuzhou 350003, Peoples R China
[2] Fujian Univ Tradit Chinese Med, Acad Integrat Med, Fuzhou 350122, Peoples R China
[3] Fujian Univ Tradit Chinese Med, Subsidiary Rehabil Hosp, Fuzhou 350003, Peoples R China
基金
中国国家自然科学基金;
关键词
electroacupuncture; neurological function; retinoic acid; cerebral ischemia-reperfusion injury; NEURAL STEM-CELLS; ADULT HIPPOCAMPAL NEUROGENESIS; OLFACTORY BULB PATHWAY; SUBVENTRICULAR ZONE; NERVOUS-SYSTEM; DENTATE GYRUS; HUMAN BRAIN; STROKE; PROLIFERATION; MICE;
D O I
10.3892/ijmm.2012.1166
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Neurogenesis is regulated by a number of signaling pathways, including the retinoic acid (RA) pathway, a key regulator of neurogenesis in the subventricular zone (SVZ) and hippocampus. Acupuncture has been used to treat neurological conditions and is known to potentially enhance cell proliferation in the neurogenic area (hippocampal dentate gyrus and the SVZ of the lateral ventricle walls) in pathological conditions, which is associated with improved brain function. However, whether or not the neuroprotective effects of electroacupuncture (EA) are mediated by the regulation of the RA signaling pathway remains to be determined. Using a transient middle cerebral artery occlusion model, in the present study we evaluated the effect of EA on the neurological functional recovery, infarction volume and investigated the underlying molecular mechanisms. Two hundred and sixteen SD rats were randomly divided into 3 groups: sham, model group (ischemic rats without EA stimulation) and EA group (ischemic rats with EA stimulation on ST36 and LI11). Behavioral deficits were detected with high-resolution digital analysis of 24-h home-cage video recordings. Infarct volume was determined by triphenyltetrazolium hydrochloride staining and the expression of RA mRNA and protein was measured using RT-PCR and western blotting, respectively. We found that EA decreased the infarct volume, promoted neurological functional recovery and increased the RA mRNA and protein expression, compared with the model group. Findings of this study suggest that promoting neurological functional recovery by modulating RA expression in the post-ischemic brain is one of the mechanisms by which EA can be effective in the treatment of ischemic stroke.
引用
收藏
页码:225 / 231
页数:7
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