Abstract
Recently, highly anti-inflammatory metabolites (α-LCMs) of α-tocopherol (α-TOH) have shed new light on the mechanism of vitamin E. A central part of myocardial infarction (MI) is a massive pro-inflammatory response in the infarcted myocardium. Since a drop of antioxidant plasma concentration has been reported during MI, we hypothesized that application of α-TOH and α-LCMs as an actual treatment of patients suffering MI provides anti-oxidative and -inflammatory protection and preserves cardiac function. Effects of vitamin E compounds on MI have been tested using the model of cardiac ischemia reperfusion (I/R) injury in mice. Treatment with vitamin E restored ejection fraction, a marker for cardiac function, and ameliorated infarct size post-I/R via regulation of immune cell infiltration, such as neutrophils and monocytes. In addition, α-TOH and α-LCMs decreased gene and protein expression as well as production of respective signaling molecules of key pro-inflammatory pathways in vitro. Since, MI is a leading cause of death worldwide, new drugs for the treatment of I/R injury in patients with MI are highly sought-after. Our study provides a new perspective for vitamin E as a treatment and its potent metabolites as possible lead structures for the therapy of MI.
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