ethyl-ferulate and caffeic-acid-phenethyl-ester

In recent years there has been a growing interest, supported by a large number of experimental and epidemiological studies, in the beneficial effects of some commonly used food-derived products in preventingvarious age-related pathologic conditions, ranging from cancer to neurodegenerative diseases. Spices and herbs often contain active phenolic substances endowed with potent antioxidative and chemopreventive properties. Curcumin is a phytochemical compound extracted from the rhizome of Curcuma Longa. It is the pigment responsible for the characteristic yellow color of Indian curry. Data from our and other laboratories demonstrated that curcumin, as well as some other polyphenols, strongly induce heme oxygenase 1 and Phase II detoxification enzymes in neurons and, by this activation, protect neurons against different modes of oxidative challenge. The potential role of curcumin as a preventive agent against brain aging and neurodegenerative disorders has been recently reinforced by epidemiological studies showing that in India, where this spice is widely used in the daily diet, there is a lower incidence of Alzheimer's disease than in the USA. These studies identify a novel class of compounds that could be used for therapeutic purposes as preventive agents against the acute neurodegenerative conditions that affect many in the world's increasingly ageing population.

Topics: Aging; Antioxidants; Brain; Caffeic Acids; Catechin; Curcumin; Diet; Flavonoids; Neurodegenerative Diseases; Neuroprotective Agents; Phenols; Phenylethyl Alcohol; Polyphenols

It is an important therapeutic strategy to protect mitochondria from oxidative stress, especially during ischemia-reperfusion. In the present study, an attempt has been made to evaluate the protective effects of caffeic acid phenethyl ester (CAPE) and its related phenolic compounds on mouse brain and liver mitochondria injury induced by in vitro anoxia-reoxygenation. Added before anoxia or reoxygenation, CAPE markedly protected coupled respiration with the decrease in state 4 and the increases in state 3, respiratory control ratio (RCR) and ADP/O ratio in a concentration-dependent manner. CAPE effectively protected mitochondria by inhibiting the mitochondrial membranes fluidity decrease, the lipoperoxidation and the protein carbonylation increase, which indicated its protective action against the mitochondrial oxidative damage. Meanwhile, CAPE blocked the enhanced release of cardiolipin (CL) and cytochrome c (Cyt c). The related phenolic compounds like caffeic acid (CA), ferulic acid (FA) and ethyl ferulate (EF) also had different-degree protective effects. CAPE and CA were more potent than FA and EF. Their structural differences played the key role in their activity levels. These results suggest that CAPE and its related phenolic compounds protect mitochondria mainly correlated to their antioxidative activities and may be of interest for the prevention and therapy of ischemia-reperfusion injuries.

Topics: Anaerobiosis; Animals; Anisotropy; Antioxidants; Brain; Caffeic Acids; Coumaric Acids; Cytochromes c; Dose-Response Relationship, Drug; Male; Mice; Mitochondria; Mitochondria, Liver; Mitochondrial Membranes; Molecular Structure; Oxygen; Phenylethyl Alcohol; Thiobarbituric Acid Reactive Substances