Bilirubin May Provide Protection Against Heart Attacks

A new study suggests that unconjugated bilirubin (UCB), an endogenous antioxidant, may protect the heart against ischemia reperfusion injury.

Researchers at Griffith University (Nathan, Australia) conducted a study in isolated Langendorff perfused hearts to test whether pre- or post-ischemic treatment with bilirubin ditaurate (BRT) improves post-ischemic functional outcomes and myocardial oxidative damage. The isolated, ex-vivo rat hearts were treated with 50 μM of BRT for 30 minutes before or after zero-flow ischemia. Functional outcomes were monitored, with myocardial damage estimated from creatine kinase efflux, infarct size, and left ventricular lipid/protein oxidation.

The results showed significant cardioprotection upon BRT treatment, with post-ischemic recoveries for left end-diastolic pressure and left ventricular developed pressure, (LVDP) significantly enhanced in the treated groups; myocardial infarction (MI) was also significantly reduced with BRT treatment. According to the researchers, the significant reductions in infarct size and lipid and protein oxidation indicate a mechanism related to protection from oxidative damage and point toward the potential of this molecule as a post-MI treatment. The study was published in the January 2016 issue of the International Journal of Cardiology.

“Inflammation is the main culprit of damage to the body, and is caused by over-active white blood cells that release free radicals. It appears our natural bilirubin can protect from these free radicals during chronic inflammatory diseases like cardiovascular disease, kidney disease, and diabetes,” said lead author Andrew Bulmer, MD. “We believe that this protection could be related to recently identified anti-oxidative property of the bilirubin molecule.”

“The findings could have positive implications for reducing health risks and improving life expectancy as a result of increasing the bilirubin concentration in people who have low levels of the pigment in blood,” added Dr. Bulmar. “Not only is there a benefit in being able to use bilirubin as a biomarker for measuring people’s future risk of various chronic diseases, there is a very real possibility it could be used as a treatment after a heart attack to reduce damage to the heart and possibly improve survival.”

Bilirubin is the yellow pigmented breakdown product of heme catabolism, caused by the body's clearance of aged red blood cells (RBCs), which contain hemoglobin. It is excreted in bile and urine, and elevated levels may indicate certain diseases. Bilirubin is responsible for the yellow color of bruises and the yellow discoloration in jaundice. It is also responsible for the brown color of feces, via its conversion to stercobilin, and the background straw-yellow color of urine via its breakdown product, urobilin.

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