Formononetin may protect aged hearts from ischemia/reperfusion damage by enhancing autophagic degradation

Myocardial infarction is a leading cause of mortality worldwide, and timely blood/oxygen reperfusion may substantially improve the outcome of infarction. However, ischemia/reperfusion (I/R) may cause severe side effects through excess reactive oxygen species generation. To develop novel methods to relieve I/R induced cell damage, the present study used a component of traditional Chinese medicine. In the present study, isolated heart tissue from aged mice and H9C2 cells with chemically-induced aging were used as experimental subjects, and it was demonstrated that formononetin was able to alleviate I/R-induced cell or tissue apoptosis. By applying formononetin to I/R-damaged tissue or cells, it was demonstrated that formononetin was able to enhance autophagy and thus alleviate I/R-induced cell damage. Furthermore, it was observed that I/R was able to inhibit lysosomal degradation processes in aged tissues or cells by impairing the lysosome acidification level, and formononetin was able to reverse this process via the re-acidification of lysosomes. In conclusion, the present study demonstrated that formononetin was able to alleviate I/R-induced cellular apoptosis in aged cells by facilitating autophagy.