Conclusions
AR facilitated EAM development, and targeting AR with ASC-J9 attenuated cardiac injury and dysfunction by inhibiting macrophages polarization towards M1 macrophages.
Results
In our study, we found that AR was increased in the myocardium and was associated with the time-course of EAM progression, which motivated us to use ASC-J9 (an enhancer of AR degradation). The results revealed that ASC-J9 administration in EAM mice resulted in an attenuation in the severity of disease and cardiac injury, a reduced CD4+T cell response, reduced monocyte/macrophage infiltration, and decreases in the pro-inflammatory cytokines. Furthermore, ASC-J9 was also found to prevent Raw264.7 cells polarization to M1 macrophages in response to LPS by upregulating suppressor of cytokine signaling 1(SOCS1) and downregulating signal transducer and activator of the transcription 5(STAT5) activity. Conclusions: AR facilitated EAM development, and targeting AR with ASC-J9 attenuated cardiac injury and dysfunction by inhibiting macrophages polarization towards M1 macrophages.