Suppr超能文献

探讨骨髓间充质干细胞通过靶向 miR-449a 调控 NF-κB 信号通路改善周围神经损伤炎症反应的机制。

Study on the Mechanism of BMSCs in Regulating NF-κB Signal Pathway by Targeting miR-449a to Improve the Inflammatory Response to Peripheral Nerve Injury.

机构信息

Department of Neurology, The Second Affiliated Hospital of Qiqihar Medical College, China.

Department of General Surgery, Qiqihar First Hospital, China.

出版信息

J Musculoskelet Neuronal Interact. 2022 Dec 1;22(4):546-561.

Abstract

OBJECTIVE

To evaluate the mechanism of Bone Marrow Mesenchymal Stem Cells (BMSCs) in regulating NF-κB signal pathway by targeting miR-449a.

METHODS

Stem cells were transfected by over-expressing and inhibiting miR-449a to detect the levels and viability of miR-449a in stem cells after transfection. Stem cells and neurons were co-cultured to evaluate the mechanism of stem cells over-expressing miR-449a on neurons.

RESULTS

After the addition of neurons, the neuronal activity of miR-449a over-expression group increased significantly, the expression of NF-κB signal pathway proteins (IκBα, p50, and p65) decreased, and the inflammatory cytokines (TNF-α and IL-1β) decreased significantly (P<0.05). experiments in rats also showed that rats were unresponsive, did not chirp or elude after being stimulated. After stem cell therapy, the weight and response of rats gradually returned to normal levels. miR-449a expression significantly increased in the stem cell + miR-449a over-expression group, expression of NF-κB signal pathway proteins (IκBα, p50, and p65) decreased, inflammatory cytokines (TNF-α and IL-1β) significantly decreased, and cell activity significantly increased (P<0.05).

CONCLUSIONS

BMSCs can modulate NF-κB signaling pathway by targeting miR-449a, so as to reduce the inflammatory response to peripheral nerve injury and repair nerve injury.

摘要

目的

通过靶向 miR-449a 来评估骨髓间充质干细胞(BMSCs)调节 NF-κB 信号通路的机制。

方法

通过过表达和抑制 miR-449a 转染干细胞,检测转染后干细胞中 miR-449a 的水平和活力。将干细胞与神经元共培养,以评估干细胞过表达 miR-449a 对神经元的作用机制。

结果

加入神经元后,miR-449a 过表达组神经元活性明显增加,NF-κB 信号通路蛋白(IκBα、p50 和 p65)表达减少,炎症细胞因子(TNF-α 和 IL-1β)明显减少(P<0.05)。大鼠实验也表明,刺激后大鼠无反应,不鸣叫或躲避。干细胞治疗后,大鼠的体重和反应逐渐恢复正常水平。在干细胞+miR-449a 过表达组中,miR-449a 的表达显著增加,NF-κB 信号通路蛋白(IκBα、p50 和 p65)的表达减少,炎症细胞因子(TNF-α 和 IL-1β)显著减少,细胞活性显著增加(P<0.05)。

结论

BMSCs 可以通过靶向 miR-449a 调节 NF-κB 信号通路,从而减轻周围神经损伤的炎症反应,修复神经损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90dc/9716300/5bde5cafe44c/JMNI-22-546-g001.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验