Affiliation:
1. Department of Orthopedics, Fourth Medical Center of the General Hospital of CPLA, Beijing, 100048, China
Abstract
SCI (SCI) poses a challenge to nerve cell repair strategies. SCI injury can lead to the development of inflammation, which in turn can exacerbate nerve cell damage. The TLR4/NF-kappa B signaling pathway is a common inflammatory signaling pathway. Since BMSCs are involved in injury repair,
whether they can promote the repair of SCI neuronal cells have not been reported. Spinal cord nerve cells were cultured in vitro and divided into mechanical injury group and BMSCs group followed by analysis of cell proliferation activity and detection of altered apoptotic activity.
Changes in the concentrations of IL-6 and IL-1β were measured by ELISA and cellular mitochondrial alterations was assessed by JG-B staining along with analysis of NF-kappa B, TLR4, related neurodevelopmental factor BDNF, and NGF expression by western blot. Mechanical damage to
neuronal cells resulted in decreased cell proliferation, increased apoptotic activity, decreased cellular mitochondrial activity, increased TLR4 and NF-kappa B expression, decreased BDNF and NGF expression, as well as increased secertions of IL-6 and IL-1β (P < 0.05).
In contrast, co-culture with BMSCs resulted in increased proliferation and decreased apoptosis of mechanically injured neuronal cells, increased cellular mitochondrial activity, with observation of the inverse changes in other factors (P < 0.05). In conclusion, BMSCs can suppress
inflammation and promote repair of injured neuronal cells by inhibiting TLR4/NF-kappa B signaling.
Publisher
American Scientific Publishers
Subject
Biomedical Engineering,Medicine (miscellaneous),Bioengineering,Biotechnology