Cardioprotection against IschemiaReperfusion by Licochalcone B in Isolated Rat Hearts

Abstract EN

The generation of reactive oxygen species (ROS) is a major cause of heart injury induced by ischemia-reperfusion.

The left ventricular developed pressure (LVDP) and the maximum up/down rate of left ventricular pressure ( ± d p / d t max ) were documented by a physiological recorder.

Myocardial infarct size was estimated macroscopically using 2,3,5-triphenyltetrazolium chloride staining.

Coronary effluent was analyzed for lactate dehydrogenase (LDH) and creatine kinase (CK) release to assess the degree of cardiac injury.

The levels of C-reactive protein (CRP), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) were analyzed to determine the inflammation status of the myocardial tissue.

Cardiomyocyte apoptosis analysis was performed using the In Situ Cell Death Detection Kit, POD.

Accordingly, licochalcone B pretreatment improved the heart rate (HR), increased LVDP, and decreased CK and LDH levels in coronary flow.

SOD level and GSH/GSSG ratio increased, whereas the levels of MDA, TNF-α, and CRP and activities of IL-8 and IL-6 decreased in licochalcone B-treated groups.

The infarct size and cell apoptosis in hearts from licochalcone B-treated group were lower than those in hearts from the I/R control group.

Therefore, the cardioprotective effects of licochalcone B may be attributed to its antioxidant, antiapoptotic, and anti-inflammatory activities.