Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2016) 43 OC6 | DOI: 10.1530/endoabs.43.OC6

WCTD2016 Abstract Topics Cardiovascular Outcome Studies (12 abstracts)

Nootkatone from Cyperus rotundus Protects Against Ischemia-reperfusion Mediated Acute Myocardial Injury in the Rat

Dong-Ung Lee 2 & Ki Churl Chang 1


1Department of Pharmacology, School of Medicine and Institute of Cardiovascular, Gyeongsang National University, South Korea; 2Division of Bioscience, Dongguk University, South Korea.


Background: Myocardial infarction is a common type of ischemic heart disease, which is the leading cause of disease-related death worldwide. In the ischemic heart, cardiac damage is initiated by a diminished blood supply, and swift restoration of blood supply is imperative to minimize cardiac injury. However, reperfusion itself can induce additional injury in the form of cardiac dysfunction, reperfusion arrhythmia, and by exacerbating myocardial infarction.

Objective: The up-regulation of heme oxygenase-1 (HO-1) has been reported to protect from I/R injury, and nootkatone, a pharmacologically active ingredient found in the rhizomes of Cyperus rotundus, has been reported to induce HO-1 in immune cells. The aim of the present study was to determine whether the protective effect of nootkatone against myocardial ischemia–reperfusion (I/R) injury is due to its antioxidant and anti-inflammatory effects.

Methods and results: Adult male rats were subjected to 30 min of ischemia and 24 h of reperfusion. Rats were randomized to receive vehicle or nootkatone (5 or 10 mg/kg) 1 h before reperfusion. Infarct sizes were measured and myocardial functions assessed. Nootkatone at 10 mg/kg i.p., significantly reduced infarct sizes vs an I/R control group and ameliorated I/R-induced myocardial dysfunction by increasing the first derivative (±dp/dt) of left ventricular pressure and by decreasing infarct size.

Conclusion: The study suggests nootkatone protects hearts from I/R injury by reducing oxidative stress and the expressions of inflammatory mediators.

Article tools

My recent searches

No recent searches.