Enriching neural stem cell and anti-inflammatory glial phenotypes with electrical stimulation after traumatic brain injury in male rats.
Enriching neural stem cell and anti-inflammatory glial phenotypes with electrical stimulation after traumatic brain injury in male rats.
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DOI：
10.1002/jnr.24834
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发表时间：
2021-07
影响因子：
4.2
通讯作者：
Bellamkonda RV
中科院分区：
文献类型：
--
作者：
Park E;Lyon JG;Alvarado-Velez M;Betancur MI;Mokarram N;Shin JH;Bellamkonda RV
外伤性脑损伤（TBI）由外部物理冲击导致脑功能受损，通过不希望的神经元死亡。损伤后，驻留和外周免疫细胞、星形胶质细胞和神经干细胞（NSCs）共同促进脑损伤后神经元功能的恢复。然而，在创伤性脑损伤急性期，免疫细胞过度的促炎反应和损伤部位内源性NSCs的消失会加剧创伤性脑损伤的进展，导致不完全愈合。因此，积极的结果可能取决于早期干预，以控制损伤早期阶段的损伤相关细胞环境。在这里，我们在啮齿动物模型（雄性Sprague-Dawley大鼠）中探索电刺激（ES）损伤部位，以研究其在TBI急性期对组成脑细胞表型和组成的总体影响。我们的数据显示，在TBI后第2天，通过CD206表达评估，短暂ES 1小时可促进小胶质细胞的抗炎表型，并在TBI后7天增加NSCs和Nestin+星形胶质细胞的数量。此外，与未受刺激的对照组相比，ES有效地增加了活神经元的数量。鉴于小胶质细胞和神经干细胞在TBI后愈合中的显著作用，我们的研究结果强烈支持在TBI急性期使用ES治疗来调节神经炎症和增强神经再生的潜在益处。创伤性脑损伤后的电刺激可增加抗炎小胶质细胞、神经干细胞和巢蛋白+星形胶质细胞的数量。
Traumatic brain injury (TBI) by an external physical impact results in compromised brain function via undesired neuronal death. Following the injury, resident and peripheral immune cells, astrocytes, and neural stem cells (NSCs) cooperatively contribute to the recovery of the neuronal function after TBI. However, excessive pro‐inflammatory responses of immune cells, and the disappearance of endogenous NSCs at the injury site during the acute phase of TBI, can exacerbate TBI progression leading to incomplete healing. Therefore, positive outcomes may depend on early interventions to control the injury‐associated cellular milieu in the early phase of injury. Here, we explore electrical stimulation (ES) of the injury site in a rodent model (male Sprague–Dawley rats) to investigate its overall effect on the constituent brain cell phenotype and composition during the acute phase of TBI. Our data showed that a brief ES for 1 hr on day 2 of TBI promoted anti‐inflammatory phenotypes of microglia as assessed by CD206 expression and increased the population of NSCs and Nestin+ astrocytes at 7 days post‐TBI. Also, ES effectively increased the number of viable neurons when compared to the unstimulated control group. Given the salience of microglia and neural stem cells for healing after TBI, our results strongly support the potential benefit of the therapeutic use of ES during the acute phase of TBI to regulate neuroinflammation and to enhance neuroregeneration. Electrical stimulation after traumatic brain injury increases population of anti‐inflammatory microglia, neural stem cells, and Nestin+ astrocytes.
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