ellagic acid/경색증

OBJECTIVE The objective was to evaluate the protective effect of ellagic acid against experimentally induced cardiac arrhythmias, hypertrophy and its association with altered lipid metabolism during myocardial infarction in rats. METHODS Rats were treated with ellagic acid (7.5 and 15 mg/kg) orally

In the paper, we observed the effect of ellagic acid (EA) on myocardial morphology and cardiac function and explored the mechanism of miR-140-3p-mediated EA in ventricular remodeling. The experimental animals were divided into 3 groups: control group, AMI group, AMI+EA group. Intragastric

Previous studies have shown that vascular endothelium-derived matrix metalloproteinases (MMPs) contribute to the destabilization of atherosclerotic plaques, a key event triggering acute myocardial infarction. In addition, studies have reported that the PKC-MEK-PPARγ signaling pathway is involved in

The preventive effect of argatroban, a synthetic thrombin inhibitor, on cerebral infarction was evaluated with ellagic acid (EA)-induced cerebral thromboembolism in rats. Platelet-rich thrombi containing fibrin and EA crystal were formed in the microarteries in the affected hemisphere by the

Our previous study described the cardioprotective effects of ellagic acid in an isoproterenol-induced myocardial infarction model. In this study, we are reporting the mechanism of protective action of ellagic acid with respect to apoptosis and mitochondrial respiratory enzymes. Ellagic acid (7.5 and

The cardioprotective property of ellagic acid in rats has been reported previously. The present study reveals the protective role of ellagic acid in biochemical parameters including serum iron, plasma iron binding capacity, uric acid, glycoprotein, and electrolytes along with hematological

The aim of this study is to research the effects of the polyphenol ellagic acid (EA) on brain cells and to explore its mechanism of action, and to evaluate whether EA can be safely utilized by humans as a functional food or therapeutic agent. A photothrombosis-induced model of brain injury in rats

The anti lipid peroxidative and antioxidant effects of ellagic acid against isoproterenol-induced myocardial infarcted rats were reported previously. This study was designed to evaluate the protective effects of ellagic acid on the levels of cardiac troponin-T, lysosomal enzymes, and membrane bound

BACKGROUND Ischemic stroke is a common cause of human disability and death. Animal models of focal cerebral ischemia are widely utilized to mimic human ischemic stroke. Although models of focal cerebral ischemia have been well established, very few evidence is based on triggering the intrinsic

Cerebral ischemia/reperfusion (I/R) injury causes a larger population of disable patients and deaths annually. Three Tibetan prescriptions have been applied in alleviating the I/R injury for a 1,000 years. Interestingly, ellagic acid (EA) is one of the commonly dominated phytochemicals in these 3

An oxygen-glucose deprivation and reoxygenation model in primary cultured rat cortical neurons was developed for this study to investigate the effects of ellagic acid (EA), a low-molecular-weight polyphenol, on neuron cells and their function, and to evaluate whether EA can be safely utilized by

The present study was designed to evaluate the cardioprotective effects of ellagic acid against isoproterenol induced myocardial infarction in rats by studying electrocardiography, blood pressure, cardiac markers, lipid peroxidation, antioxidant defense system and histological changes. Male Wistar

Cardiac fibroblasts (CFs) could be activated after myocardial infarction (MI). Thus, it is necessary to explore effective drugs to suppress the activation of CFs following MI. This study was designed to investigate the impacts of ellagic acid on CFs and the underlying mechanisms. The expression of

Neuroinflammation contributes to neuronal death in cerebral ischemia. Urolithin A (UA), a gut microbial metabolite of ellagic acid, has emerged as a potential anti-inflammatory agent. However, its roles and precise mechanisms in stroke remain unknown. Here we found that UA treatment ameliorated