Background

Intracerebral hemorrhage (ICH) stands as the most fatal stroke subtype, lacking any specific therapeutic approach yielding benefits for functional recovery.

Objectives

We aimed to explore the involvement of long non-coding RNA small nucleolar RNA host gene 3 (lncRNA-SNHG3) in post-ICH neuroinflammation, offering a novel rationale for ICH treatment.

Results

Brain tissues of ICH-induced mice exhibited upregulated levels of lncRNA-SNHG3. Inhibition of lncRNA-SNHG3 led to reduced modified neurological severity scores, diminished brain edema, and attenuated inflammatory infiltration, coupled with reduced levels of tumor necrosis factor-α/interleukin-1β. By repressing miR-106b-5p via targeted binding, lncRNA-SNHG3 facilitated the inhibition of transcriptional and protein levels of thioredoxin-interacting protein (TXNIP) through targeted binding to TXNIP mRNA. The counteraction of miR-106b-5p inhibition or the upregulation of TXNIP reversed the ameliorative effect of sh-SNHG3 on neuroinflammation.

Conclusion

Competitive binding of lncRNA-SNHG3 to miR-106b-5p resulted in the upregulation of TXNIP, consequently inducing neuroinflammation and exacerbating ICH-induced damage.

中文翻译：

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LncRNA-SNHG3通过调节miR-106b-5p/TXNIP轴促进脑出血后神经炎症

背景

脑出血（ICH）是最致命的中风亚型，缺乏任何有利于功能恢复的具体治疗方法。

目标

我们的目的是探索长链非编码RNA小核仁RNA宿主基因3（lncRNA-SNHG3）在ICH后神经炎症中的参与，为ICH治疗提供新的原理。

结果

ICH 诱导的小鼠脑组织表现出 lncRNA-SNHG3 水平上调。抑制lncRNA-SNHG3可降低神经系统严重程度评分，减轻脑水肿，减轻炎症浸润，同时降低肿瘤坏死因子-α/白细胞介素-1β的水平。通过靶向结合抑制 miR-106b-5p，lncRNA-SNHG3 通过靶向结合 TXNIP mRNA 促进硫氧还蛋白相互作用蛋白 (TXNIP) 转录和蛋白水平的抑制。miR-106b-5p 抑制或 TXNIP 上调的抵消作用逆转了 sh-SNHG3 对神经炎症的改善作用。

结论

lncRNA-SNHG3 与 miR-106b-5p 的竞争性结合导致 TXNIP 上调，从而诱导神经炎症并加剧 ICH 诱导的损伤。