Mesenchymal stem cells mitigate inflammatory response in BV2 microglial cells caused by radiation via modulating toll-like receptor signal pathway
10.3760/cma.j.issn.1671-8925.2017.03.010
- VernacularTitle:间充质干细胞通过调控TLR信号通路减轻放射所致BV2小胶质细胞炎症反应
- Author:
Huan LIAO
1
;
Hongxuan WANG
;
Ying PENG
Author Information
1. 广州市中山大学孙逸仙纪念医院神经科
- Keywords:
Mesenchymal stem cell;
Microglia;
Radiation-induced brain injury;
Toll-like receptor signal pathway
- From:
Chinese Journal of Neuromedicine
2017;16(3):269-273
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of human mesenchymal stem cells (MSCs) on changes of toll-like receptor (TLR) signal pathway in BV2 microglial cells caused by radiation.Methods Human MSCs and BV2 microglial cells were cultured routinely.The experiment included four groups (un-irradiated BV2 control group,un-irradiated BV2 plus MSCs treatment group,irradiated BV2 group,irradiated BV2 plus MSCs treatment group).A single dose of 10 Gy was given to BV2 cells.BV-2 and MSCs co-culture experiments were performed through Transwell co-culture system with MSCs (105 per upper insert) and BV2 (2×105 per lower well).Quantitative real-time PCR (qRT-PCR) was applied for investigating the mRNA expressions of interleukin (IL)-6,tumor necrosis factor (TNF)-α,TLR2 and TLR4.ELISA kits were used to measure the protein expressions of IL-6 and TNF-α.Results The qRT-PCR showed that the IL-6 and TNF-α mRNA expressions in the irradiated BV2 group were significantly increased as compared with those in the un-irradiated BV2 control group (P＜0.05);the IL-6 and TNF-α mRNA expressions in the irradiated BV2 group were significantly increased as compared with those in the irradiated BV2 plus MSCs treatment group (P＜0.05);ELISA indicated similar results.The qRT-PCR results suggested that MSCs could decrease the TLR4 and TLR2 mRNA expressions in the irradiated BV2 cells.Conclusion MSCs can mitigate the inflammatory response in microglial cells induced by radiation through modulating the related factors in TLR signal pathway.
