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miRNA-146a 在癫痫持续状态大鼠炎症反应中的作用。

Involvement of microRNA-146a in the Inflammatory Response of S tatus Epilepticus Rats.

机构信息

Department of Neurology, Jinshan Hospital, Fudan University, Shanghai 201508. China.

Department of Cerebropathy, The Second Affiliated Hospital, Hunan University of Traditional Chinese Medicine, Changsha 410005. China.

出版信息

CNS Neurol Disord Drug Targets. 2017;16(6):686-693. doi: 10.2174/1871527316666170505123956.

DOI:10.2174/1871527316666170505123956
PMID:28474544
Abstract

BACKGROUND

Status epilepticus (SE), is characterized by high mortality and morbidity, which can cause neuronal injury, neuronal death and alteration of neuronal networks, Recently, inflammation was shown to play a significant role in SE pathogenesis. And miRNA-146a has been shown to be involved in inflammation and to inhibit inflammatory cytokines through NF-κB pathway. In our study, we investigated the relationship between inflammation and miR-146a expression.

METHOD

The SE rat model was induced by lithium-pilocarpine. Hematoxylin and eosin staining (H&E) was performed to observe the histopathology of the rat hippocampus. The expression of COX-2, TNF-α, IL-6 and IL-1β were respectively measured by Western blot and Bio-Plex ProTM Assays. The miR-146a expression in hippocampus tissue was measured by Quantitative real-time PCR.

RESULTS

microRNA-146a was highly expressed in the hippocampus of SE rats coupled with increased level of inflammatory cytokines than the normal group. And TQ can attune the expression of inflammatory cytokines, meanwhile, miR-146a was lower in TQ group. The expression of miRNA-146a were positively correlated with the level of inflammatory reaction.

CONCLUSION

TQ may alleviate the inflammatory reaction by inhibiting the NF-κB signaling pathway. Our study shows that miRNA-146a was involved in the inflammatory response and indicated inflammation severity in SE rats. Therefore, miRNA-146a may serve as a potential biomarker or a therapeutic target in SE.

摘要

背景

癫痫持续状态(SE)的特征是高死亡率和发病率,可导致神经元损伤、神经元死亡和神经元网络改变。最近,炎症被证明在 SE 的发病机制中起重要作用。miR-146a 已被证明参与炎症,并通过 NF-κB 途径抑制炎症细胞因子。在我们的研究中,我们研究了炎症与 miR-146a 表达之间的关系。

方法

锂-匹罗卡品诱导 SE 大鼠模型。苏木精和伊红染色(H&E)观察大鼠海马的组织病理学。Western blot 和 Bio-Plex ProTM 测定分别测定 COX-2、TNF-α、IL-6 和 IL-1β 的表达。定量实时 PCR 测定海马组织中 miR-146a 的表达。

结果

miR-146a 在 SE 大鼠海马中高度表达,伴有炎症细胞因子水平升高,高于正常组。TQ 可以调节炎症细胞因子的表达,同时 TQ 组 miR-146a 水平较低。miR-146a 的表达与炎症反应水平呈正相关。

结论

TQ 可能通过抑制 NF-κB 信号通路减轻炎症反应。我们的研究表明,miR-146a 参与了炎症反应,并表明 SE 大鼠的炎症严重程度。因此,miR-146a 可能作为 SE 的潜在生物标志物或治疗靶点。

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