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

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

DOI:
10.1177/1545968320948065
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发表时间:
2020-08-10
影响因子:
4.2
通讯作者:
Feng, Zhen
Feng, Zhen
中科院分区:
医学1区
文献类型:
--
作者:
Tang, Yunliang;Dong, Xiaoyang;Feng, Zhen

文献摘要

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背景。外伤性脑损伤(TBI)是世界范围内造成死亡和残疾的主要原因。氧化应激、炎症和细胞凋亡是创伤性脑损伤后重要的病理生理特征。目标。研究表明,迷走神经刺激(VNS)可以减轻多种疾病的氧化应激。然而,VNS在TBI中的关键作用仍未完全了解。本研究探讨了VNS对TBI的保护作用及其可能机制。方法雄性Sprague-Dawley大鼠随机分为假手术组、TBI组和TBI + VNS组。采用自由落体法建立大鼠脑损伤模型。分离迷走神经干,建立TBI模型后行VNS观察。结果。结果显示,与假VNS组相比,VNS显著改善了组织损伤、神经功能缺损和脑水肿。此外,VNS还能减轻大鼠脑外伤后突周皮层氧化应激、炎症和细胞凋亡。VNS还显著抑制核因子κ B (nf - κ B)蛋白在细胞核中的表达和核苷酸结合结构域样受体蛋白3 (NLRP3)炎症小体的激活。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,可能通过NF-kappa B/NLRP3信号通路减轻脑损伤后的脑损伤。
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-kappa B (NF-kappa B) 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-kappa B/NLRP3 signaling pathway.