Honokiol Protects against Anti-ß1-Adrenergic Receptor Autoantibody-Induced Myocardial Dysfunction via Activation of Autophagy.

Myocardial diseases are prevalent syndromes with high mortality rate. The exploration of effective interference is important. Anti-ß1-adrenergic receptor autoantibody (ß1-AAB) is highly correlated with myocardial dysfunction. The actions and underlying mechanisms of honokiol (HNK) in ß1-AAB-positive patients await to be unraveled. In this study, we established a rat model of ß1-AAB positive with myocardial dysfunction. Cardiac function following ß1-AR-ECII administration was analyzed using the VisualSonics Vevo 770 High-Resolution In Vivo Imaging System. The levels of autophagy-related proteins were detected by Western blotting. Our data revealed that HNK reversed ß1-AAB-induced effects and protected myocardial tissues from dysfunction. After HNK treatment, the cardiac contractile ability increased and the LDH activity decreased. HNK attenuated myocardial degeneration. In addition, HNK promoted the activation of the AMP-dependent protein kinase/Unc-51-like autophagy activating kinase (AMPK/ULK) pathway and activated autophagy. These results suggest that HNK protects against ß1-AAB-induced myocardial dysfunction via activation of autophagy and it may be a potentially therapeutic compound for ß1-AAB-positive myocardial diseases.