Cyanidin ameliorates endotoxin-induced myocardial toxicity by modulating inflammation and oxidative stress through mitochondria and other factors.

Cyanidin, an anthocyanin pigment, demonstrates anti-oxidant and anti-inflammatory properties. Here, we examined the mechanistic role of cyanidin in endotoxin induced myocardial injury in inflammation and oxidative stress. In lipopolysaccharide (LPS) induced myocardial injury model, cyanidin ameliorated cardiac injury (Lactate dehydrogenase or LDH, Creatine Kinase or CK, cardiac troponin I or cTnI and cardiac myosin light chains 1 or cMLC1), cell death (caspase 3 activity and PARP activity), and improved cardiac function (ejection fraction or EF and end diastolic left ventricular inner dimension or LVID).