Transcranial direct current stimulation alleviated ischemic stroke induced injury involving the BDNF-TrkB signaling axis in rats

作者全名："Zhou, Qinxiang; Chen, Yu; Tang, Hao; Zhang, Lei; Ma, Yue; Bai, Dingqun; Kong, Yuhan"

作者地址："[Zhou, Qinxiang; Chen, Yu; Zhang, Lei; Ma, Yue; Bai, Dingqun; Kong, Yuhan] Chongqing Med Univ, Affiliated Hosp 1, Dept Rehabil Med, Chongqing, Peoples R China; [Zhou, Qinxiang; Chen, Yu; Tang, Hao; Kong, Yuhan] Chongqing Key Lab Neurol, Chongqing, Peoples R China; [Tang, Hao] Chongqing Med Univ, Affiliated Hosp 2, Dept Neurol, Chongqing, Peoples R China; [Zhang, Lei; Ma, Yue] Chongqing Med Univ, Affiliated Hosp 1, Dept Neurol, Chongqing, Peoples R China"

通信作者："Bai, DQ; Kong, YH (通讯作者)，Chongqing Med Univ, Affiliated Hosp 1, Dept Rehabil Med, Chongqing, Peoples R China."

来源：HELIYON

ESI学科分类：　

WOS号：WOS:001000508200001

JCR分区：Q1

影响因子：3.4

年份：2023

卷号：9

期号：4

开始页：　

结束页：　

文献类型：Article

关键词：Ischemic stroke; Transcranial direct current stimulation; BDNF; TrkB; MCAO; R; Apoptosis

摘要："Ischemic stroke causes a complicated sequence of apoptotic cascades leading to neuronal damage and functional impairments. Transcranial direct current stimulation (tDCS) is a non-invasive treatment technique that uses electrodes to deliver weak current to the head. It could influence brain activity and has a crucial role in neuronal survival and plasticity. The current study investigated the neuroprotective effects and potential mechanisms of tDCS by brain-derived neurotrophic factor (BDNF) and its related receptor tropomyosin-receptor kinase B (TrkB) against apoptosis following ischemic injury in vivo.The effect of consecutive treatment with tDCS for seven days on rats after Middle cerebral artery occlusion/reperfusion (MCAO/R) surgery was studied. Western blotting, immunofluores-cent staining, TUNEL assay, and electron microscope were conducted seven days after tDCS treatment, and the motor function was assessed at 1, 3, and 7 days. Activities of BDNF-TrkB signaling axis and apoptosis-related proteins were determined in the cerebral cortex. At seven days after tDCS treatment, it increased BDNF levels and promoted the regeneration of axons compared with the MCAO/R group. There was also a reduction in neuronal apoptosis and improved functional deficits. Whereafter, a TrkB receptor inhibitor K252a was administrated to clarify whether the neuroprotection of tDCS is exerted via BDNF-TrkB signaling. The results depicted that K252a application significantly inhibited the neuroprotection impact of tDCS treatment. It was accompanied by a significant downregulation of phosphorylation of TrkB, PI3K, and Akt.Our study investigated the neuroprotective effects of tDCS against ischemic injury. The results indicate that upregulation of BDNF and its critical receptor TrkB, as well as its downstream PI3K/ Akt pathway, were involved in the protective effects exerted by tDCS."

基金机构："National Natural Science Foundation of China [81401865]; Chongqing Science and Technology commission [cstc2019jcyj-msxmX0339]; Program for Innovation Team Building at Institutions of Higher Education in Chongqing [CXQT21018]; Program for Youth Innovation in Future Medicine, Chongqing Medical University [W0076]"

基金资助正文："Yuhan Kong was supported by the National Natural Science Foundation of China [81401865], and the Chongqing Science and Technology commission [cstc2019jcyj-msxmX0339]. Dingqun Bai was supported by Program for Innovation Team Building at Institutions of Higher Education in Chongqing [CXQT21018], and Program for Youth Innovation in Future Medicine, Chongqing Medical University [W0076]."