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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. [Display omitted] • Cerebral ischemia-reperfusion activates multiple apoptotic pathways. • Direct current stimulation could control hyperthermia and hyperglycemia. • Direct current stimulation could weaken apoptosis pathways and enhance cerebral recovery. • Using direct current stimulation could improve learning and memory disorders. • Cathodal and anodal currents during ischemia-reperfusion could induce more neuroprotection. [ABSTRACT FROM AUTHOR]

• The decrease in the cerebral blood flow activates several pathophysiological pathways in cerebral ischemia. • Previously, no intervention stimulation was performed in the stage of cerebral ischemia. • A single immediate use of tDCS attenuated the several physiopathological pathways during cerebral ischemia, especially in the cathodal type (c/tDCS). Global cerebral ischemia (CI) causes severe neuronal injury, mainly in the hippocampal CA1 region. This study aimed to investigate an immediate using transcranial direct current stimulation (tDCS) in reducing neuronal injury induced by CI. The 32 Wistar male rats were randomly divided into four groups (n=8 per group). In the ischemia group (I), CI was induced via the 4-vessel occlusion model. In the sham group (Sh), rats did not receive any intervention. In the ischemia+cathodal group (I+c/tDCS), the cathodal current was applied during CI. In the ischemia+anodal group (I+a/tDCS), the anodal current was applied. The current intensity of 400 μA was applied for 15-min during the ischemia. Hippocampal tissue was used to assess levels of NMDAR, IL-1β, TNF-α, MDA, SOD, NOS, and apoptosis markers. Histological assessment and TUNEL staining were performed in CA1 hippocampal region. The c/tDCS significantly decreased the levels of IL-1β and TNF-α than the I and a/tDCS groups. The c/tDCS significantly reduced MDA and NOS levels, while increasing the level of SOD than the I and a/tDCS. The c/tDCS caused a significant decrease in NMDAR level than the a/tDCS. Using c/tDCS significantly reduced the Bax and Caspase-3 expressions, while increasing the Bcl-2 expression than the I group. In the c/tDCS group, DNA fragmentation and neuronal death were significantly lower than the I and a/tDCS groups. Using cathodal a direct current could attenuate primary pathophysiological pathways induced by CI, and it eventually reduced neurons death and apoptosis in the CA1 hippocampal region. [ABSTRACT FROM AUTHOR]