Cardioprotection against Ischemia/Reperfusion by Licochalcone B in Isolated Rat Hearts

Abstract

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 (±dp/dt 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.

Naringin protects against anoxia/reoxygenation-induced apoptosis in H9c2 cells via the Nrf2 signaling pathway

“…34 In accordance with a previous study, 35 our present study demonstrated that A/R exposure significantly increased ROS production in H9c2 cells, thereby increasing the levels of MDA, which is an oxidative stress marker (Fig. 34 In accordance with a previous study, 35 our present study demonstrated that A/R exposure significantly increased ROS production in H9c2 cells, thereby increasing the levels of MDA, which is an oxidative stress marker (Fig.…”

Rosmarinic Acid Protects against Inflammation and Cardiomyocyte Apoptosis during Myocardial Ischemia/Reperfusion Injury by Activating Peroxisome Proliferator-Activated Receptor Gamma

“…Along these lines, inflammation plays a key role in cardiac I/R injury, and the harmful reactions that follow these reactions include an elevated release of proinflammatory cytokines (such as CRP, TNF-α and IL-6) (Han et al, 2014; Li and Ye, 2015). Studies have demonstrated that several chemically distinct agonists of PPARγ reduce myocardial infarct size caused by regional I/R in rats (Goyal et al, 2011; Hu Q. et al, 2014).…”

Cardioprotective Effect of Losartan Alone or in Combination with Remote Ischemic Preconditioning on the Biochemical Changes Induced by Ischemic/Reperfusion Injury in a Mutual Prospective Study with a Clinical and Experimental Animal Arm

“…17,18 In our study; Losartan pretreatment in animal model of I/Rat a dose of 20 mg/kg/day for 6 weeks before induction of I/R achieved a biochemical cardioprotective effect through reduction of I/R induced elevation of IL-6, TNF-α and CRP. Angiotensin II is described as a potent pro-inflammatory mediator causing up regulation of macrophages to induce inflam- 19 Furthermore, angiotensin II has been found to have a dual effect on macrophages through activation of the mitogenactivated protein kinase (MAPK) pathway and up-regulation of early growth response-1 (Egr-1) gene expression which both master the switch for vascular inflammatory responses.…”

“…On the contrary, lowering of CK-MB levels was reported in the effluent liquid of an isolated heart model linked to langend off reperfused apparatus where the heart was pretreated with valsartan before induction of I/R. 26 The discrepancy in losartan effect on CK-MB levels between the two animal models may be ascribed to the difference in study design where our model was in vivo, while the other study 26 was in vitro. In vitro model of I/R allowed direct perfusion of the ang II blocker (valsartan) to the heart while in our study losartan was administered orally, so in vitro model may achieve better availability of the drug to the heart than in vivo model.…”