TY - JOUR AB - Spinal cord injury (SCI) results in inflammation, and TLR4, which is an inflammatory factor, has an important role in the pathological injury that occurs following SCI. Recently, bone marrow stromal cells (BMSCs) have been demonstrated to be a novel treatment in SCI. However, the underlying mechanism of neuroprotection in SCI by BMSCs remains unclear. The present study was designed to investigate the therapeutic mechanism of BMSCs in SCI by analysis of Toll‑like receptor 4 (TLR4)/nuclear factor‑κB (NF‑κB) expression. The present results demonstrated that BMSC transplantation promoted functional recovery and tissue repair in SCI rats. Interestingly, it also reduced the expression of TLR4 and NF‑κB after SCI. Furthermore, it was demonstrated that BMSCs downregulated the expression of apoptosis factor caspase‑12 in the SCI rat model. The present results demonstrated that BMSCs may have incorporated into the spinal cord to improve locomotor function after SCI, partly via the TLR4/NF‑κB signaling pathway. To the best of our knowledge, this is the first study to determine that BMSCs prevented secondary injury and enhanced functional recovery in SCI via inhibition of TLR4/NF‑κB‑mediated inflammation. AD - Department of Anatomy, School of Medicine, Taizhou University, Taizhou, Zhejiang 317000, P.R. China School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310058, P.R. China AU - Bai,Shi AU - Zhou,Hao AU - Wu,Lijuan DA - 2019/01/01 DO - 10.3892/etm.2018.6907 EP - 448 IS - 1 JO - Exp Ther Med KW - spinal cord injury bone marrow stromal cells inflammation nuclear factor‑κB Toll‑like receptor‑4 PY - 2019 SN - 1792-0981 1792-1015 SP - 444 ST - Bone marrow stromal cells improved functional recovery in spinal cord injury rats partly via the Toll‑like receptor‑4/nuclear factor‑κB signaling pathway T2 - Experimental and Therapeutic Medicine TI - Bone marrow stromal cells improved functional recovery in spinal cord injury rats partly via the Toll‑like receptor‑4/nuclear factor‑κB signaling pathway UR - https://doi.org/10.3892/etm.2018.6907 VL - 17 ER -