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

• Published in: Molecular medicine reports Vol. 18; no. 6; pp. 4821 - 4830
• Main Authors: Huang, Zhengxin, Liu, Yingfeng, Huang, Xianping
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications UK Ltd 01.12.2018; D.A. Spandidos
• Subjects: Acidification; Aging; Animals; Apoptosis; Apoptosis - drug effects; Autophagy; Autophagy - drug effects; Biomarkers; Cell Line; Cellular Senescence - drug effects; Heart attacks; Heart Function Tests; Ischemia; Isoflavones - pharmacology; Kinases; Laboratory animals; Lysosomes; Lysosomes - metabolism; Male; Medical research; Mice; Myocardial infarction; Myocardial Reperfusion Injury - drug therapy; Myocardial Reperfusion Injury - metabolism; Myocardial Reperfusion Injury - pathology; Myocardial Reperfusion Injury - physiopathology; Phagocytosis; Protective Agents - pharmacology; Proteins; Reactive oxygen species; Reperfusion; Rodents; Traditional Chinese medicine; Traditional medicine; United States > US; ischemia/reperfusion; autophagy; aging cells; Chinese traditional medicine; formononetin
• ISSN: 1791-2997; 1791-3004; 1791-3004
• DOI: 10.3892/mmr.2018.9544

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.