Background

Spinal cord injury (SCI) is a devastating disease that can lead to tissue loss and neurological dysfunction. TNIP2 is a negative regulator of NF-κB signaling due to its capacity to bind A20 and suppress inflammatory cytokines-induced NF-κB activation. However, the anti-inflammatory role of TNIP2 in SCI remains unclear. Our study's intention was to evaluate the effect of TNIP2 on the inflammatory response of microglia after spinal cord injury in rats.

Methods

HE staining and Nissl staining were performed on day 3 following SCI to analyze the histological changes. To further investigate the functional changes of TNIP2 after SCI, we performed immunofluorescence staining experiments. The effect of LPS on TNIP2 expression in BV2 cells was examined by western blot. The levels of TNF-α, IL-1β, and IL-6 in spinal cord tissues of rats with SCI and in BV2 cells with LPS were measured by using qPCR.

Results

TNIP2 expression was closely associated with the pathophysiology of SCI in rats, and TNIP2 was involved in regulating functional changes in microglia. TNIP2 expression was increased during SCI in rats and that overexpression of TNIP2 inhibited M1 polarization and pro-inflammatory cytokine production in microglia, which might ultimately protect against inflammatory responses through the MAPK and NF-κB signaling pathways.

Conclusions

The present study provides evidence for a role of TNIP2 in the regulation of inflammation in SCI and suggests that induction of TNIP2 expression alleviated the inflammatory response of microglia.

中文翻译：

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TNIP2对大鼠脊髓损伤后小胶质细胞炎症反应的保护作用

背景

脊髓损伤(SCI) 是一种破坏性疾病，可导致组织损失和神经功能障碍。TNIP2 能够结合 A20 并抑制炎症细胞因子诱导的 NF-κB 激活，因此是 NF-κB 信号传导的负调节因子。然而，TNIP2 在 SCI 中的抗炎作用仍不清楚。我们的研究目的是评估 TNIP2 对大鼠脊髓损伤后小胶质细胞炎症反应的影响。

方法

SCI后第3天进行HE染色和尼氏染色以分析组织学变化。为了进一步研究 SCI 后 TNIP2 的功能变化，我们进行了免疫荧光染色实验。通过蛋白质印迹法检测LPS对BV2细胞中TNIP2表达的影响。采用 qPCR 检测 SCI 大鼠脊髓组织和 LPS BV2 细胞中 TNF-α、IL-1β 和 IL-6 的水平。

结果

TNIP2的表达与大鼠SCI的病理生理密切相关，TNIP2参与调节小胶质细胞的功能变化。大鼠 SCI 期间 TNIP2 表达增加，TNIP2 的过度表达抑制小胶质细胞中 M1 极化和促炎细胞因子的产生，这可能最终通过 MAPK 和 NF-κB 信号通路防止炎症反应。

结论

本研究为 TNIP2 在 SCI 炎症调节中的作用提供了证据，并表明诱导 TNIP2 表达可减轻小胶质细胞的炎症反应。