TRIM44沉默通过下调TLR4-NF-κB信号通路抑制炎症,减轻大鼠创伤性脑损伤

IF 2.2 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM Neuroimmunomodulation Pub Date : 2022-01-01 DOI:10.1159/000524536
Lin Zhu, Ce Dong, Xiongfei Yue, Pengzhen Ge, Guozhen Zheng, Zhanying Ye, Baogen Pan
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引用次数: 0

摘要

背景:创伤性脑损伤(TBI)后的神经炎症对患者的康复非常重要,并且与TBI后的神经退行性改变有关。tripartite motif containing 44 (TRIM44)蛋白是一种E3连接酶,参与免疫功能的调节,与TBI没有已知的联系。本研究探讨了TRIM44与TBI之间的联系。方法:对照皮质损伤诱导大鼠TBI后,采用实时定量逆转录聚合酶链反应和Western blot检测TRIM44的表达,并通过TLR4表达、p65磷酸化、NF-κB特异性转录活性检测toll样受体4 (TLR4)-NF-κB信号通路。通过检测促炎细胞因子和TLR4-NF-κB信号分子、改善神经系统严重程度评分、脑含水量和Evans蓝通透性,揭示TRIM44敲低对TBI大鼠炎症、神经功能和TLR4-NF-κB信号的影响。结果:我们发现TRIM44在TBI诱导后表达显著升高,TLR4-NF-κB被激活。沉默TRIM44可抑制TBI大鼠的促炎细胞因子产生,改善神经预后,减轻脑水肿,抑制TLR4-NF-κB信号传导。结论:我们的研究结果表明,抑制TRIM44或调节相关通路可能是TBI的一种治疗策略。
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Silencing of TRIM44 Inhibits Inflammation and Alleviates Traumatic Brain Injury in Rats by Downregulating TLR4-NF-κB Signaling.

Background: Neuroinflammation subsequent to traumatic brain injury (TBI) is important for the recovery of patients and is associated with neurodegenerative changes post-TBI. The tripartite motif containing 44 (TRIM44) protein is an E3 ligase involved in the regulation of immune function with no previously known link to TBI. This study explores the connection between TRIM44 and TBI.

Methods: After induction of TBI in rats by control cortex injury, TRIM44 expressions were determined with quantitative real-time reverse transcription polymerase chain reaction and Western blot, and Toll-like receptor 4 (TLR4)-NF-κB signaling was examined by the expression of TLR4, p65 phosphorylation, and the specific NF-κB transcription activity. The effects of TRIM44 knockdown on inflammation, neurological function, and TLR4-NF-κB signaling in TBI rats were revealed by the detection of proinflammatory cytokines and TLR4-NF-κB signaling molecules, modified neurological severity score, brain water content, and Evans blue permeability.

Results: We found that TRIM44 expression was significantly increased following TBI induction along with TLR4-NF-κB activation. Silencing of TRIM44 suppressed proinflammatory cytokine production, improved neurological outcomes, alleviated brain edema, and inhibited TLR4-NF-κB signaling in TBI rats.

Conclusion: Our findings suggest that suppressing TRIM44 or modulation of relevant pathways may be a therapeutic strategy for TBI.

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来源期刊
Neuroimmunomodulation
Neuroimmunomodulation 医学-免疫学
CiteScore
3.60
自引率
4.20%
发文量
35
审稿时长
>12 weeks
期刊介绍: The rapidly expanding area of research known as neuroimmunomodulation explores the way in which the nervous system interacts with the immune system via neural, hormonal, and paracrine actions. Encompassing both basic and clinical research, ''Neuroimmunomodulation'' reports on all aspects of these interactions. Basic investigations consider all neural and humoral networks from molecular genetics through cell regulation to integrative systems of the body. The journal also aims to clarify the basic mechanisms involved in the pathogenesis of the CNS pathology in AIDS patients and in various neurodegenerative diseases. Although primarily devoted to research articles, timely reviews are published on a regular basis.
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