A hypothesis: Edaravone exert cardioprotection partly via modulation of adiponectin.

Edaravone has been recognized as a potential protective agent for cardiovascular diseases. It is well known that edaravone can attenuate oxidative stress and inhibit the production of proinflammatory cytokines such as TNF-α. However, the mechanisms behind the cardioprotection of edaravone are still incompletely understood yet. As a primary adipose-derived protein, adiponectin exhibits protective properties on the heart and blood vessels. Accumulative studies have shown that there exists a reciprocal relationship between adiponectin and TNF-α, i.e., adiponectin negatively regulates TNF-α expression, whereas adiponectin expression is inhibited by TNF-α. So we hypothesize that edaravone plays a role in cardioprotection partly through modulation of adiponectin level by suppression of TNF-α.