Edaravone promotes A1/A2 polarization of astrocytes through JAK2 / STAT3 pathway

Abstract

Abstract Edaravone is widely used in acute stroke. Regulation of astrocyte activation by edaravone is thought to be one of the neuroprotective mechanisms of neuroprotection of edaravone after ischemic injury. Previous studies have shown that astrocytes are rapidly activated after cerebral ischemia and differentiation into a neuroprotective A1 phenotype and a damaging A2 phenotype. Therefore, the present study aim to find the effects of edaravone on the A1/A2 phenotype of activated astrocytes after cerebral ischemia and the underlying regulatory mechanisms. For this purpose, we replicated the cerebral ischemia model and the oxygen-glucose deprivation induced astrocytes model. Western blot and immunofluorescence were used to detect the expression changes of A1 astrocyte markers C3 and SerpinG1, and A2 astrocyte markers PTX3 and SPHK1, respectively. We found that edaravone could significantly decreased the expression of C3 and SerpinG1 and enhanced PTX3 and SPHK1 expression in A2 astrocytes. Importantly, the JAK2/STAT3 pathway was activated after astrocyte activation, and edaravone treatment significantly inhibited the expression of proteins associated with this pathway. In light of the above, edaravone can promote the transformation of A1 astrocytes to A2 phenotype by regulating JAK2/STAT3 pathway and play a neuroprotective role.