Electro-acupuncture up-regulates astrocytic MCT1 expression to improve neurological deficit in middle cerebral artery occlusion rats

被引:19
|
作者
Lu, Yan [1 ]
Zhao, Haijun [1 ]
Wang, Yuan [1 ]
Han, Bingbing [1 ]
Wang, Tong [2 ]
Zhao, Hong [3 ]
Cui, Kemi [3 ]
Wang, Shijun [1 ]
机构
[1] Shandong Univ Tradit Chinese Med, Coll Acumox & Tuina, Dept Expt Acupunctuiol, Jinan 250355, Shandong, Peoples R China
[2] Shandong Univ Tradit Chinese Med, Sch Nursing, Jinan 250355, Shandong, Peoples R China
[3] Cornell Univ, Weill Med Coll, Houston Methodist Res Inst, Dept Syst Med & Bioengn, Houston, TX 77030 USA
基金
中国国家自然科学基金;
关键词
Electro-acupuncture (EA); Middle cerebral artery occlusion (MCAO); Focal cerebral ischemia; Monocarboxylate transporter (MCT); Astrocyte; Lactate metabolism; GLUCOSE-UTILIZATION; ACUPUNCTURE; ISCHEMIA; MODEL;
D O I
10.1016/j.lfs.2015.05.014
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
Aims: Cerebral ischemia is one of the common diseases treated by electro-acupuncture (EA). Although the clinical efficacy has been widely affirmed, the mechanisms of action leading to the health benefits are not understood. In this study, the role of EA in modulating the lactate energy metabolism and lactate transportation was explored on the middle cerebral artery occlusion (MCAO) ischemic rat model. Main methods: Repeated EA treatments once daily for 7 days were applied to the MCAO rats and neurological function evaluation was performed. Brain tissues were harvested for lactate concentration examination, immunohistochemical staining. Western blot and oRT-PCR analyses for the expressions of lactate transporter (monocarboxylate transporter 1, MCT1) and glial fibrillary acidic protein (GFAP). Key findings: The animal behavioral tests showed that the 7-day EA treatments significantly promoted the recovery of neurological deficits in the MCAO rats, which correlated with the enhanced lactate energy metabolism in the ischemic brain. In the cortical ischemic area of the MCAO rats, EA treatments led to the activation of astrocytes, and induced a further increase of lactate transporter (monocarboxylate transporter I, MCT1) expression in astrocytes at both protein and mRNA levels. Significance: Our results suggest that the EA treatments activated lactate metabolism in the resident astrocytes around the ischemic area and up-regulated the expression of MCT1 in these astrocytes which facilitated the transfer of intracellular lactate to extracellular domain to be utilized by injured neurons to improve the neurological deficit. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:68 / 72
页数:5
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