| Literature DB >> 28962170 |
Ruhui Lin1, Xiaojie Li2, Weilin Liu3, Wenlie Chen1, Kunqiang Yu4, Congkuai Zhao4, Jia Huang3, Shanli Yang4, Hongwei Peng4, Jing Tao3, Lidian Chen3.
Abstract
A previous study by our group found that electro-acupuncture (EA) at the Shenting (DU24) and Baihui (DU20) acupoints ameliorates cognitive impairment in rats with cerebral ischemia-reperfusion (I/R) injury. However, the precise mechanism of action has remained largely unknown. The present study investigated whether brain-derived neurotropic factor (BDNF) mediates hippocampal synaptic plasticity as the underlying mechanism. Rats were randomly divided into three groups: The sham operation control (Sham) group, the focal cerebral ischemia-reperfusion (I/R) group, and the I/R with EA treatment (I/R+EA) group. The I/R+EA group received EA treatment at the Shenting (DU24) and Baihui (DU20) acupoints after the operation. EA treatment was found to ameliorate neurological deficits (P<0.05) and reduce the cerebral infarct volume (P<0.01). In addition, EA improved cognitive function in cerebral I/R-injured rats (P<0.05). Furthermore, EA treatment promoted synaptic plasticity. Simultaneously, EA increased the hippocampal expression of BDNF, its high-affinity tropomyosin receptor kinase B (TrkB) and post-synaptic density protein-95 (PSD-95) in the rats with cerebral I/R injury. Collectively, the findings suggested that BDNF-mediated hippocampal synaptic plasticity may be one mechanism via which EA treatment at the Shenting (DU24) and Baihui (DU20) acupoints improves cognitive function in cerebral I/R injured rats.Entities:
Keywords: brain-derived neurotropic factor; cerebral ischemia-reperfusion; cognitive impairment; electro-acupuncture; synaptic plasticity
Year: 2017 PMID: 28962170 PMCID: PMC5609168 DOI: 10.3892/etm.2017.4750
Source DB: PubMed Journal: Exp Ther Med ISSN: 1792-0981 Impact factor: 2.447