Background Transcranial direct current stimulation (tDCS) is a non-invasive brain modulation technique that has been proved to exert beneficial effects in the acute phase of stroke. To explore the underlying mechanism, we investigated the neuroprotective effects of cathodal tDCS on brain injury caused by middle cerebral artery occlusion (MCAO). Results We established the MCAO model and sham MCAO model with an epicranial electrode implanted adult male Sprague–Dawley rats, and then they were randomly divided into four groups (MCAO + tDCS, MCAO + sham tDCS (Sham), Control + tDCS and Control + Sham group). In this study, the severity degree of neurological deficit, the morphology of brain damage, the apoptosis, the level of neuron-specific enolase and inflammatory factors, the activation of glial cells was detected. The results showed that cathodal tDCS significantly improved the level of neurological deficit and the brain morphology, reduced the brain damage area and apoptotic index, and increased the number of Nissl body in MCAO rats, compared with MCAO + Sham group. Meanwhile, the high level of NSE, inflammatory factors, Caspase 3 and Bax/Bcl2 ratio in MCAO rats was reduced by cathodal tDCS. Additionally, cathodal tDCS inhibited the activation of astrocyte and microglia induced by MCAO. No difference was found in two Control groups. Conclusion Our results suggested that cathodal tDCS could accelerate the recovery of neurologic deficit and brain damage caused by MCAO. The inhibition of neuroinflammation and apoptosis resulted from cathodal tDCS may be involved in the neuroprotective process.

中文翻译：

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阴极 tDCS 在急性缺血性卒中后对大鼠脑发挥神经保护作用

背景经颅直流电刺激 (tDCS) 是一种非侵入性大脑调制技术，已被证明在中风急性期发挥有益作用。为了探索潜在的机制，我们研究了阴极 tDCS 对大脑中动脉闭塞 (MCAO) 引起的脑损伤的神经保护作用。结果 我们建立了 MCAO 模型和假 MCAO 模型，植入了颅外电极的成年雄性 Sprague-Dawley 大鼠，然后将它们随机分为四组（MCAO + tDCS、MCAO + sham tDCS（Sham）、Control + tDCS 和 Control +假组）。本研究检测了神经功能缺损的严重程度、脑损伤的形态、细胞凋亡、神经元特异性烯醇化酶和炎症因子的水平、胶质细胞的活化情况。结果表明，与MCAO+Sham组相比，阴极tDCS显着改善了MCAO大鼠的神经功能缺损水平和脑形态，减少了脑损伤面积和凋亡指数，增加了Nissl小体数量。同时，阴极 tDCS 降低了 MCAO 大鼠的高水平 NSE、炎症因子、Caspase 3 和 Bax/Bcl2 比值。此外，阴极 tDCS 抑制了 MCAO 诱导的星形胶质细胞和小胶质细胞的活化。在两个对照组中没有发现差异。结论 我们的结果表明，阴极 tDCS 可以加速 MCAO 引起的神经功能缺损和脑损伤的恢复。阴极tDCS对神经炎症和细胞凋亡的抑制可能参与了神经保护过程。