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OBJECTIVE
To observe the protective effects of catechin morphon (GCG and EGCG) on hypoxia-reoxygenation induced injury in myocardial cells and to explore the mechanisms.
METHODS
In cultured neonatal rat cardiomyocytes, we investigated the preconditioning protection by GCG and EGCG on the spontaneous
Background: Myocardial infarction (MI) is a serious condition, caused by acute, persistent ischemia or hypoxia of a coronary artery and responsible for heart failure and sudden death. This study aimed to investigate the effects of catechin, one of the main active components of green tea, on
BACKGROUND
The intermittent hypoxia (IH) that characterizes sleep-disordered breathing impairs spatial learning and increases NADPH oxidase activity and oxidative stress in rodents. We hypothesized that green tea catechin polyphenols (GTPs) may attenuate IH-induced neurobehavioral deficits by
Defective activation and proliferation in microglial cells has been suggested to be associated with the increase of cerebral ischemia/reperfusion injury. We investigated the protection and molecular mechanism of green tea catechin on hypoxia/reperfusion-induced microglial cell injury in vitro.
Catechin protects heart from myocardial ischaemia/reperfusion (MI/R) injury. However, whether catechin inhibits H/R-induced myocardial cell apoptosis is largely unknown.This study aims to investigate the underlying mechanism of catechin in inhibiting the The amyloid-degrading enzyme neprilysin (NEP) is one of the therapeutic targets in prevention and treatment of Alzheimer's disease (AD). As we have shown previously NEP expression in rat parietal cortex (Cx) and hippocampus (Hip) decreases with age and is also significantly reduced after prenatal
Catechins have recently been reported to increase the cellular content of the hypoxia-inducible factor (HIF)-1alpha within mammalian cells. These catechins have a gallate moiety as a common structure. We now report that n-propyl gallate (nPG) also increases the HIF-1alpha protein in the rat
Focal and segmental glomerular sclerosis (FSGS) is a common cause of nephrotic syndrome and end-stage renal disease. It has been reported that overproduction of reactive oxygen species (ROS) and cell apoptosis are associated with the development of FSGS. Epigallocatechin-3-gallate Tacrine is an acetylcholinesterase inhibitor approved for the treatment of Alzheimer's disease. Unfortunately, reversible hepatotoxicity in about 30% of patients at therapeutic doses limits clinical use. The purpose of this study was to develop and characterize a model of tacrine hepatotoxicity to
The antinecrotic potential of a new drug, 3-palmitoyl-(+)-catechin (PC), which is a derivative of (+)-cyanidanol-3, was studied in two different experimental models of necrosis of the liver in the rat: acute hepatitis induced by galactosamine and liver damage induced by a combination of chronic
Hypoxia-inducible factor-1 (HIF-1) is a transcription factor that induces oxygen-regulated genes in response to reduced oxygen conditions (hypoxia). Expression of the oxygen-regulated HIF-1alpha subunit correlates positively with advanced disease stages and poor prognosis in cancer patients. Green
Catechin-rich green tea extract (GTE) protects against nonalcoholic steatohepatitis (NASH) by alleviating gut-derived endotoxin translocation and hepatic Toll-like receptor-4 (TLR4)-nuclear factor κB (NFκB) inflammation. We hypothesized that intact GTE would attenuate NASH-associated responses along
Tea, the most widely consumed natural beverage has been associated with reduced mortality risk from cardiovascular disease. Oolong tea is a partially fermented tea containing high levels of catechins, their degree of oxidation varies between 20%-80% causing differences in their active metabolites.
It has previously been demonstrated that phosphatidylinositol-3-kinase (PI3K)/Akt and cleaved caspase-3 serve critical roles in the apoptosis of cardiac myocytes following ischemia/reperfusion injury. Epigallocatechin-3-gallate (EGCG), the predominant catechin component of green tea, has been
Surgical correction of congenital cardiac malformations mostly implies the use of cardiopulmonary bypass (CPB). However, a possible negative impact of CPB on cerebral structures like the hippocampus cannot be neglected. Therefore, we investigated the effect of CPB on hippocampus CA1 and CA3 regions