Cathodal tDCS exerts neuroprotective effect in rat brain after acute ischemic stroke
Cathodal tDCS exerts neuroprotective effect in rat brain after acute ischemic stroke
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DOI：
10.1186/s12868-020-00570-8
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发表时间：
2020-05-12
期刊：
影响因子：
2.4
通讯作者：
Ding, Gui-Rong
中科院分区：
文献类型：
--
作者：
Zhang, Ke-Ying;Rui, Gang;Ding, Gui-Rong
经颅直流电刺激（tDCS）是一种非侵入性脑调节技术，已被证明在脑卒中急性期发挥有益作用。为了探讨其潜在机制，我们研究了阴极tDCS对大脑中动脉闭塞（MCAO）脑损伤的神经保护作用。结果采用外颅电极植入成年雄性sd大鼠，建立MCAO模型和假性MCAO模型，随机分为MCAO + tDCS组、MCAO +假性tDCS组（sham）、Control + tDCS组和Control + sham组。本研究检测了大鼠神经功能缺损的严重程度、脑损伤形态、细胞凋亡、神经元特异性烯醇化酶和炎症因子水平、神经胶质细胞活化情况。结果显示，与MCAO + Sham组相比，阴极tDCS可显著改善MCAO大鼠神经功能缺损程度和脑形态，减少脑损伤面积和凋亡指数，增加Nissl小体数量。同时，tDCS可降低MCAO大鼠高水平的NSE、炎性因子、Caspase 3和Bax/Bcl2比值。此外，阴极tDCS抑制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。结论阴极tDCS可加速MCAO所致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。
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.