The First People's Hospital of Foshan, Foshan, Guangdong, China.
Deja Lab, Foshan, Guangdong, China.
Mol Biol Rep. 2024 Aug 28;51(1):941. doi: 10.1007/s11033-024-09878-8.
Traumatic brain injury (TBI) is a major cause of neurological disability, and current treatments have limited effectiveness. Recent studies have emphasized the potential of exosomes derived from umbilical cord mesenchymal stem cells (UC-MSCs-Exo) in TBI treatment, but the molecular mechanisms underlying their therapeutic effects are not fully understood.
In this study, UC-MSCs-Exo was isolated using ultracentrifugation and intraventricularly injected to TBI rat model. The neurofunctional motor function of the rats was evaluated using the modified neurological severity score (mNSS), and the activation of microglia was assessed through immunofluorescence detection of IBA1 expression levels. Additionally, we established an in vitro neuroinflammatory model using BV2 microglia to investigate the effects of UC-MSCs-Exo and miRNA-21. Our findings indicate that UC-MSCs-Exo promote neurological recovery in TBI rats and inhibit excessive microglia activation. Furthermore, UC-MSCs-Exo highly expresses miRNA-21 and inhibited the proliferation, migration, and release of inflammatory mediators of BV2 microglia by transporting miRNA-21.
The present study suggests that the promotion of neurological recovery in TBI rats by UC-MSCs-Exo may be attributed to the inhibition of excessive microglia activation through miRNA-21.
创伤性脑损伤 (TBI) 是导致神经功能障碍的主要原因，目前的治疗方法效果有限。最近的研究强调了源自脐带间充质干细胞 (UC-MSCs-Exo) 的外泌体在 TBI 治疗中的潜力，但它们治疗效果的分子机制尚不完全清楚。
在这项研究中，使用超速离心法分离 UC-MSCs-Exo，并通过脑室注射到 TBI 大鼠模型中。使用改良神经严重程度评分 (mNSS) 评估大鼠的神经功能运动功能，通过 IBA1 表达水平的免疫荧光检测评估小胶质细胞的激活。此外，我们使用 BV2 小胶质细胞建立了体外神经炎症模型，以研究 UC-MSCs-Exo 和 miRNA-21 的作用。我们的研究结果表明，UC-MSCs-Exo 可促进 TBI 大鼠的神经恢复并抑制过度的小胶质细胞激活。此外，UC-MSCs-Exo 高度表达 miRNA-21，并通过转运 miRNA-21 抑制 BV2 小胶质细胞的增殖、迁移和炎症介质的释放。
本研究表明，UC-MSCs-Exo 促进 TBI 大鼠的神经恢复可能归因于通过 miRNA-21 抑制过度的小胶质细胞激活。
