Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Department of Anesthesiology, School of Allied Medical Sciences, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Brain Res Bull. 2022 Aug;186:70-78. doi: 10.1016/j.brainresbull.2022.05.013. Epub 2022 May 30.
Cerebral ischemia-reperfusion, subsequent hyperthermia, and hyperglycemia lead to neural damage. This study aimed to investigate the effects of using cathodal and/or anodal transcranial direct current stimulation (tDCS) in different stages of ischemia-reperfusion on apoptosis and controlling hyperthermia and hyperglycemia.
A total of 78 male Wistar rats were randomly assigned into six groups (n = 13), including sham, ischemia/reperfusion (I/R), anodal-tDCS (a-tDCS), cathodal-tDCS (c-tDCS), anodal/cathodal-tDCS (a/c-tDCS), and cathodal/anodal-tDCS (c/a-tDCS) groups. Global cerebral I/R was induced in all of the groups except for sham group. In a-tDCS and c-tDCS groups, the rats received anodal and cathodal currents in both I/R stages, respectively. In a/c-tDCS group, the rats received anodal current during the ischemia and cathodal current during the reperfusion. The c/a-tDCS group received the currents in the reverse order. The current intensity of 400 µA was applied in ischemia phase (15 min) and reperfusion phase (30 min, twice a day). Body temperature and plasma blood sugar were measured daily. Rats were also tested for novel object recognition and passive avoidance memory. The apoptosis of hippocampal tissue was evaluated by measuring Bax, Bcl-2, Caspase-3, and TUNEL staining.
All tDCS significantly reduced hyperthermia and hyperglycemia, as well as Bax and Caspase-3 levels, it also increased Bcl-2 expression. The preliminary results from c/a-tDCS mode could improve the expression of apoptotic markers, memory function, hyperthermia, and hyperglycemia control and reduce DNA fragmentation compared to other stimulatory therapies.
All tDCS modes could save neurons by suppressing apoptotic and enhancing anti-apoptotic pathways, especially in the c/a tDCS mode.
脑缺血再灌注、随后的高热和高血糖会导致神经损伤。本研究旨在探讨在缺血再灌注的不同阶段使用阴极和/或阳极经颅直流电刺激（tDCS）对细胞凋亡以及控制高热和高血糖的影响。
共 78 只雄性 Wistar 大鼠随机分为 6 组（n=13），包括假手术组、缺血再灌注组（I/R 组）、阳极 tDCS 组（a-tDCS 组）、阴极 tDCS 组（c-tDCS 组）、阳极/阴极 tDCS 组（a/c-tDCS 组）和阴极/阳极 tDCS 组（c/a-tDCS 组）。除假手术组外，所有组均诱导全脑缺血再灌注。在 a-tDCS 和 c-tDCS 组中，大鼠在 I/R 两个阶段分别接受阳极和阴极电流。在 a/c-tDCS 组中，大鼠在缺血期接受阳极电流，在再灌注期接受阴极电流。c/a-tDCS 组则相反。缺血期（15 分钟）和再灌注期（30 分钟，每天两次）应用 400µA 的电流强度。每天测量体温和血浆血糖。大鼠还进行了新物体识别和被动回避记忆测试。通过测量 Bax、Bcl-2、Caspase-3 和 TUNEL 染色评估海马组织的细胞凋亡。
所有 tDCS 均显著降低高热和高血糖以及 Bax 和 Caspase-3 水平，同时增加 Bcl-2 表达。与其他刺激疗法相比，c/a-tDCS 模式可改善凋亡标志物的表达、记忆功能、高热和高血糖的控制，并减少 DNA 片段化。
所有 tDCS 模式都可以通过抑制凋亡和增强抗凋亡途径来挽救神经元，尤其是在 c/a-tDCS 模式下。
