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迷走神经刺激通过调节 NF-κB/NLRP3 信号通路减轻早期创伤性脑损伤。

Vagus Nerve Stimulation Attenuates Early Traumatic Brain Injury by Regulating the NF-κB/NLRP3 Signaling Pathway.

机构信息

Department of Rehabilitation Medicine, First Affiliated Hospital of Nanchang University, Nanchang, People's Republic of China.

出版信息

Neurorehabil Neural Repair. 2020 Sep;34(9):831-843. doi: 10.1177/1545968320948065. Epub 2020 Aug 10.

DOI:10.1177/1545968320948065
PMID:32772884
Abstract

BACKGROUND

Traumatic brain injury (TBI) is a major cause of death and disability worldwide. Oxidative stress, inflammation, and apoptosis are vital pathophysiological features post-TBI.

OBJECTIVES

Research has shown that vagus nerve stimulation (VNS) can attenuate oxidative stress in various diseases. However, the critical role of VNS in TBI is still not completely understood. This study investigated the protective effects and potential mechanism of VNS on TBI.

METHODS

Male Sprague-Dawley rats were randomized into 3 groups: sham, TBI, and TBI + VNS. The TBI model was induced in rats by the free-fall drop method. The vagal nerve trunk was separated, and VNS was performed after establishing the TBI model.

RESULTS

The results showed that VNS significantly ameliorated tissue damage, neurological deficits, and cerebral edema, compared with the sham VNS group. Additionally, VNS alleviated oxidative stress, inflammation, and apoptosis in the pericontusive cortex of rats after TBI. VNS also significantly suppressed expression of the nuclear factor-κB (NF-κB) protein in the nucleus and activation of the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome.

CONCLUSIONS

Taken together, the present study indicates that VNS may attenuate brain damage after TBI by inhibiting oxidative stress, inflammation, and apoptosis, possibly through the NF-κB/NLRP3 signaling pathway.

摘要

背景

创伤性脑损伤(TBI)是全球范围内导致死亡和残疾的主要原因。氧化应激、炎症和细胞凋亡是 TBI 后的重要病理生理特征。

目的

研究表明,迷走神经刺激(VNS)可减轻多种疾病中的氧化应激。然而,VNS 在 TBI 中的关键作用仍不完全清楚。本研究探讨了 VNS 对 TBI 的保护作用及其潜在机制。

方法

雄性 Sprague-Dawley 大鼠随机分为 3 组:假手术组、TBI 组和 TBI+VNS 组。采用自由落体撞击法建立大鼠 TBI 模型,在建立 TBI 模型后分离迷走神经干并进行 VNS。

结果

结果显示,与假手术 VNS 组相比,VNS 显著改善了 TBI 大鼠的组织损伤、神经功能缺损和脑水肿。此外,VNS 减轻了 TBI 后大鼠皮质损伤区的氧化应激、炎症和细胞凋亡。VNS 还显著抑制了核因子-κB(NF-κB)蛋白在核内的表达和核苷酸结合寡聚结构域样受体蛋白 3(NLRP3)炎性小体的激活。

结论

综上所述,本研究表明,VNS 可能通过抑制氧化应激、炎症和细胞凋亡来减轻 TBI 后的脑损伤,其机制可能与 NF-κB/NLRP3 信号通路有关。

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