Molecular targets for anti-oxidative protection of green tea polyphenols against myocardial ischemic injury

Abstract

Ischemic heart disease is the leading cause of death worldwide. An improved understanding of the mechanisms involved in myocardial injury would allow intervention downstream in the pathway where certain drugs including natural products could be efficiently applied to target the end effectors of the cell death pathway. Green tea polyphenols (GTPs) have potent anti-oxidative capabilities, which may account for their beneficial effects in preventing oxidative stress associated with ischemia injury. Although studies have provided convincing evidence to support the protective effects of GTPs in cardiovascular system, the potential end effectors that mediate cardiac protection are only beginning to be addressed. Proteomics analyses widely used to identify the protein targets for many cardiovascular diseases have advanced the discovery of the signaling mechanism for GTPs-mediated cardio-protection. This review focuses on putative triggers, mediators, and end effectors for the GTPs-mediated cardio-protection signaling pathways engaged in myocardial ischemia crisis, allowing a promising natural product to be used for ameliorating oxidative stress associated with ischemic heart diseases.

Potential Protective Effects of Bioactive Constituents from Chinese Propolis against Acute Oxidative Stress Induced by Hydrogen Peroxide in Cardiac H9c2 Cells

“…ROS-induced effects of ischemia–reperfusion and myocardial dysfunction could be alleviated by treating the tissue with antioxidants or blocking signaling-related ROS generation. Based on this concept, several practices have been performed to evaluate the effects of antioxidants, including propolis, on myocardial injuries in animals and patients [12, 13]. …”

Early Fluid Resuscitation by Lactated Ringer’s Solution Alleviate the Cardiac Apoptosis in Rats with Trauma-Hemorrhagic Shock

“…Ischemic tissue reperfusion injury is associated with elevated ROS production and Ca 2+ overload [12]. Apoptosis is a programmed cell death, which is induced by two types of mechanisms.…”

Treatment with 17β-Estradiol Reduced Body Weight and the Risk of Cardiovascular Disease in a High-Fat Diet-Induced Animal Model of Obesity

“…These findings indicate that 17β-E treatments dose-dependently activation of ERβ may directly and the activation of ERα in 17β-E treatments may indirectly protect cardiomyocytes [31,32]. In this work, the results obtained for reasonable explanation to phytoestrogens protection in high-fat diet-fed animal hearts rather than emphasize the application of estrogen in obesity clinical therapy [33]. …”