Cabbage extract containing chlorogenic acid has notable scavenging activity against hydroxyl radicals, superoxide anion radicals, DPPH radicals as well as potent reducing power. Oral administration of the extract (240 mg/kg BW/day) to hypercholesterolaemic rats reduced by high-fat diet for 30 days lowered their blood TC, TG, and LDL-C levels by 36.3, 43.5 and 45.8%, respectively. However, the blood HDL-C levels in the same treated rats increased by 17.1%. Treatment of hypercholesterolaemic rats with the extract significantly increased the GSH level along with enhanced SOD, CAT activities in liver tissues. Furthermore, the extract significantly decreased hepatic MDA as well as GPx and GR activities in extract-treated rats. It can therefore be concluded that the extract has a high hypolipidaemic activity and this may be attributed to its antioxidative potential.

Acrolein is a highly electrophilic alpha, beta-unsaturated aldehyde to which humans are exposed in many situations and has been implicated in neurodegenerative diseases such as Alzheimer's disease. A galloyl dimer prorobinetinidin from Acacia mearnsii De Wild, robinetinidol-(4beta-->8)-epigallocatechin 3-O-gallate (REO), has antioxidant properties and could protect brain against acrolein-induced oxidative damage. In this study, the molecular basis of acrolein-induced cytotoxicity in human neuroblastoma SH-SY5Y cells and the modulating effects of REO were examined. Our results indicate that REO protects SH-SY5Y cells from acrolein-induced damage by the attenuation of reactive oxygen species, the remediation of NADPH oxidase activity, the enhancement of the glutathione system, and the prevention of protein oxidation/nitration and lipid peroxidation. In order to determine the effects of REO on mitochondrial events, mitochondrial membrane potentials (Delta Psim) and caspase cascades downstream of mitochondria were assessed. REO inhibited the collapse of Delta Psi m, suggesting that REO reduces the mitochondrial dysfunction associated with acrolein treatment. REO also inhibited caspase-3 activation, which can be triggered by mitochondrial malfunctions. Furthermore, REO induced a significant reduction in the level of phospho-JNK, which is known as an apoptotic mediator in acrolein-induced neuronal cell death. Our results indicate that REO protects neurons from the deleterious effects of acrolein via the attenuation of oxidative stress, NADPH oxidase activity, GSH depletion, protein oxidation/nitration, lipid peroxidation, mitochondrial dysfunction, JNK activation, and caspase activity. These findings suggest that REO could be potentially useful as a protective agent for people exposed to acrolein.