Traumatic brain injury (TBI) is one of the leading causes of morbidity and mortality among the world, while the advance of TBI management is rather limited in recent years. The deregulation of microRNAs (miRNAs) has been widely reported in TBI patients and animal models, and certain miRNAs have been identified as the emerging biomarkers of TBI. However, the role of miRNAs in the regulatory mechanism of TBI remains unclear. To demonstrate the effect of miR-146a mimic on TBI-induced neural damages, TBI mouse model was constructed by cortical impact injury (CCI). The chemokine levels were examined by ELISA assays. Behavioral experiments were used to estimate the impact of miR-146a mimics on neurological functions in mice. Western blot assays were performed to demonstrate the protein levels. qRT-PCR assays were utilized to investigate the expression alteration of RNA levels. It was found that miR-146a was upregulated both in brain and serum in TBI mice. miR-146a mimic downregulated inflammatory cytokines secretion in mouse brain. The NF-κB signaling pathway was inhibited by miR-146a mimic. miR-146a treatment attenuated the impact caused by TBI to mouse brain and improve the long-term neurological function. In conclusion, miR-146a mimics ameliorate TBI-related injuries via JNK and NF-κB signaling pathway.

中文翻译：

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miR-146a 模拟物可改善涉及 JNK 和 NF-κB 信号通路的创伤性脑损伤。

创伤性脑损伤（TBI）是世界上发病率和死亡率的主要原因之一，而近年来TBI管理的进展相当有限。microRNAs (miRNAs) 的失调已在 TBI 患者和动物模型中得到广泛报道，某些 miRNAs 已被确定为 TBI 的新兴生物标志物。然而，miRNA在TBI调控机制中的作用尚不清楚。为了证明 miR-146a 模拟物对 TBI 诱导的神经损伤的影响，通过皮质撞击损伤 (CCI) 构建了 TBI 小鼠模型。通过ELISA测定检查趋化因子水平。行为实验用于评估 miR-146a 模拟物对小鼠神经功能的影响。进行蛋白质印迹分析以证明蛋白质水平。qRT-PCR 检测被用来研究 RNA 水平的表达变化。发现 miR-146a 在 TBI 小鼠的脑和血清中均上调。miR-146a 模拟小鼠大脑中下调的炎性细胞因子分泌。NF-κB 信号通路被 miR-146a 模拟物抑制。miR-146a 治疗减弱了 TBI 对小鼠大脑的影响，改善了长期的神经功能。总之，miR-146a 通过 JNK 和 NF-κB 信号通路模拟改善 TBI 相关损伤。miR-146a 治疗减弱了 TBI 对小鼠大脑的影响，改善了长期的神经功能。总之，miR-146a 通过 JNK 和 NF-κB 信号通路模拟改善 TBI 相关损伤。miR-146a 治疗减弱了 TBI 对小鼠大脑的影响，改善了长期的神经功能。总之，miR-146a 通过 JNK 和 NF-κB 信号通路模拟改善 TBI 相关损伤。