小胶质细胞和星形胶质细胞的反应有助于缓解重复经颅磁刺激对创伤性脑损伤大鼠造成的炎症损伤

IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Neurochemical Research Pub Date : 2024-06-23 DOI:10.1007/s11064-024-04197-7
FangFang Qian, RenHong He, XiaoHui Du, Yi Wei, Zhou Zhou, JianZhong Fan, YouHua He
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摘要

重复经颅磁刺激(rTMS)是一种有望改善创伤性脑损伤(TBI)临床后遗症的治疗策略。这些改善与神经元及其突触连接的神经可塑性变化有关。然而,据推测,经颅磁刺激也可能调节小胶质细胞和星形胶质细胞,从而增强它们的神经保护能力。本研究旨在探讨高频经颅磁刺激对小胶质细胞和星形胶质细胞的影响,这些影响可能会促进经颅磁刺激的神经保护作用。研究采用费尼体重下降法建立中度创伤性脑损伤大鼠模型。通过观察突触超微结构和神经元凋亡水平,评估高频经颅磁刺激对大鼠神经的保护作用。通过免疫荧光染色和 Western 印迹技术评估了小胶质细胞和星形胶质细胞中几种重要的炎症相关蛋白的水平。我们的研究结果表明,通过经颅磁刺激对小胶质细胞和星形胶质细胞的调节,可以挽救损伤的神经元。这种调节在保护突触超微结构和抑制神经元凋亡方面起着关键作用。在小胶质细胞中,我们观察到经颅磁刺激抑制了促炎因子(CD16、IL-6 和 TNF-α)的水平,促进了抗炎因子(CD206、IL-10 和 TNF-β)的水平。此外,经颅磁刺激还能下调 P75NTR 的表达,上调星形胶质细胞中 IL33 的表达。这些发现表明,对小胶质细胞和星形胶质细胞的调节是经颅磁刺激减轻中度创伤性脑损伤后神经元炎症损伤的机制。
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Microglia and Astrocytes Responses Contribute to Alleviating Inflammatory Damage by Repetitive Transcranial Magnetic Stimulation in Rats with Traumatic Brain Injury

Repetitive transcranial magnetic stimulation (rTMS) is a therapeutic strategy that shows promise in ameliorating the clinical sequelae following traumatic brain injury (TBI). These improvements are associated with neuroplastic changes in neurons and their synaptic connections. However, it has been hypothesized that rTMS may also modulate microglia and astrocytes, potentially potentiating their neuroprotective capabilities. This study aims to investigate the effects of high-frequency rTMS on microglia and astrocytes that may contribute to its neuroprotective effects. Feeney’s weight-dropping method was used to establish rat models of moderate TBI. To evaluate the neuroprotective effect of high frequency rTMS on rats by observing the synaptic ultrastructure and the level of neuron apoptosis. The levels of several important inflammation-related proteins within microglia and astrocytes were assessed through immunofluorescence staining and western blot. Our findings demonstrate that injured neurons can be rescued through the modulation of microglia and astrocytes by rTMS. This modulation plays a key role in preserving the synaptic ultrastructure and inhibiting neuronal apoptosis. Among microglia, we observed that rTMS inhibited the levels of proinflammatory factors (CD16, IL-6 and TNF-α) and promoted the levels of anti-inflammatory factors (CD206, IL-10 and TNF-β). rTMS also reduced the levels of pyroptosis within microglia and pyroptosis-related proteins (NLRP3, Caspase-1, GSDMD, IL-1β and IL-18). Moreover, rTMS downregulated P75NTR expression and up-regulated IL33 expression in astrocytes. These findings suggest that regulation of microglia and astrocytes is the mechanism through which rTMS attenuates neuronal inflammatory damage after moderate TBI.

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来源期刊
Neurochemical Research
Neurochemical Research 医学-神经科学
CiteScore
7.70
自引率
2.30%
发文量
320
审稿时长
6 months
期刊介绍: Neurochemical Research is devoted to the rapid publication of studies that use neurochemical methodology in research on nervous system structure and function. The journal publishes original reports of experimental and clinical research results, perceptive reviews of significant problem areas in the neurosciences, brief comments of a methodological or interpretive nature, and research summaries conducted by leading scientists whose works are not readily available in English.
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