AUTHOR=Zou Hong-jun , Guo Shi-Wu , Zhu Lin , Xu Xu , Liu Jin-bo 

TITLE=Methylprednisolone Induces Neuro-Protective Effects via the Inhibition of A1 Astrocyte Activation in Traumatic Spinal Cord Injury Mouse Models

JOURNAL=Frontiers in Neuroscience

VOLUME=Volume 15 - 2021

YEAR=2021

URL=https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2021.628917

DOI=10.3389/fnins.2021.628917

ISSN=1662-453X

ABSTRACT=Traumatic spinal cord injury leads to pathological changes such as inflammation, edema, and neuronal apoptosis. Methylprednisolone is a glucocorticoid that has a variety of beneficial effects, including decreasing inflammation and ischemic reaction, as well as inhibiting lipid peroxidation. However, the efficacy and mechanism of Methylprednisolone in traumatic spinal cord injury therapy is yet to be deciphered. In the present study, Methylprednisolone significantly attenuated the apoptotic effects of H2O2 in neuronal cells. Western blot analysis demonstrated that the levels of apoptotic related proteins, Bax and cleaved caspase-3, were reduced while levels of anti-apoptotic Bcl-2 were increased. In vivo TUNEL assays further demonstrated that Methylprednisolone effectively protected neuronal cells from apoptosis after traumatic spinal cord injury, and was consistent with in vitro studies. Furthermore, we demonstrated that MP could decrease expression levels of IBA1, Il-1α, TNFα, and C3 and suppress A1 neurotoxic reactive astrocyte activation in traumatic spinal cord injury mouse models. Neurological function was evaluated using the Basso Mouse Scale and Footprint Test. Results demonstrated that the neurological function of MP-treated injured mice was significantly increased. In conclusion, our study demonstrated that Methylprednisolone could attenuate astrocyte cell death, decrease microglia activation and promote functional recovery after acute traumatic spinal cord injury in mouse models.