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It is believed that these benecial effects of green tea polyphenols are the result of their potent antioxidative properties.In the central nervous system, there is also some evidence to show that oral administration of green tea polyphenols and avonoidrelated compounds has preventive effects on ironinduced lipid peroxide accumulation and agerelated accumulation of neurotoxic lipid peroxides in the rat brain are usually expected to be scavengers of free radicals, but different components have different functions.We investigated the effects of exposure of PC cells to OHDA alone or associated with pretreatment with TC.Exposure of PC cells to OHDA induced a concentrationdependent decrease in cell viability determined by assay and apoptosis of PC cells observed by ow cytometry, uorescence microscopy, and DNA fragmentation technique.From to M, the protective effects increased with the concentrations and EGCG was better than green tea polyphenols at the same concentrations.MPTP neurotoxin caused dopamine neuron loss in substantia nigra concomitant with a depletion in striatal dopamine and tyrosine hydroxylase protein levels.Pretreatment with either green tea extract prevented these effects.In addition, the neurotoxin caused an elevation in striatal antioxidant enzymes superoxide dismutase activities, both effects being prevented by ECG.ECG also increased the activities of both enzymes in the brain.The neuroprotective effects are not likely to be caused by the inhibition of MPTP conversion to its active metabolite methylphenylpyridinium by monoamine oxidaseB, as both green tea and ECG are very poor inhibitors of this enzyme in vitro. The brainpenetrating property of polyphenols, as well as their antioxidant and ironchelating properties, might make such compounds an important class of drugs to be developed for treatment of neurodegenerative diseases where oxidative stress has been implicated and black tea induced lipid peroxidation.Introduction of GT extract before OHDA inhibited both NFB nuclear translocation and binding activity induced by this toxin in SHSYY cells.However, the neuroprotective effect of EGCG on cell survival was abolished by pretreatment with PKC inhibitor GF X. Because EGCG increased phosphorylated PKC, they suggest that PKC isoenzymes are involved in the neuroprotective action of EGCG against OHDA.These results suggest that the neuroprotective mechanism of EGCG against oxidativestressinduced cell death includes stimulation of PKC and modulation of cell survivalcell cycle genes are usually expected to be a potent chemopreventive agent because of their scavenging free radicals and chelating metal ions ability.The existing data strongly suggest that the soy isoavones have a protective action against several chronic diseases such as atherosclerosis, the diseases associated with postmenopausal estrogen deciency, and hormonedependent breast and prostate cancers reported that genitein protected rat brain synatosome from insult induced by A.Genistein, a phytoestrogen capable of crossing the bloodbrain barrier and chemicals. It was found that exposure to aged A for hincreased the DCF uorescence intensity twofold relative to controls.The {|Targetmol’s {Endurobol|Amiodarone increase in DCF uorescence intensity was eliminated by when cotreated with genistein at M and aged A, whereas genistein at. M decreased about of the production of ROS induced by A.Therefore, genistein at a high concentration has stronger antioxidative activities in comparison with a low concentration in the prevention of neuronal cell death induced by A.

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