title: Modulation of the oxidative stress and nuclear factor kappaB activation by theaflavin 3,3'-gallate in the rats exposed to cerebral ischemia-reperfusion.
abstract: The major pathobiological mechanisms of IR injury include excitotoxicity, oxidative stress, and inflammation. TF3, a major constituent of black tea, possesses biological functions such as anti-oxidative and anti-inflammatory activities. The purpose of this study was to verify the neuronal protective potential of TF3 and its mechanisms against cerebral IR injury in rats. TF3 administration (10 and 20 mg.kg-1) ameliorated the infarct volume. TF3 also decreased the content of MDA and NO. TF3 significantly increased the activity of SOD and GSH-Px, which were reduced by IR injury. Administration of TF3 decreased mRNA and protein expression of COX-2 and iNOS. DNA binding and Western blotting revealed an increase in NF-kappaB activation and IkappaB depletion in IR brain tissue. Pretreatment with TF3 markedly inhibited IRinduced increase in nuclear localization of NF-kappaB, and preserved IkappaB in the cytoplasm. The results show that TF3 exerts protective effects against cerebral IR injury by reducing oxidative stress and modulating the NF-kappaB activation.
authors.affiliation: Department of Pharmacology, Medical College, Xianning University, Xianning, People's Republic of China.
authors.forename: F
authors.initials: F
authors.lastname: Cai
authors.forename: C
authors.initials: C
authors.lastname: Li
authors.forename: J
authors.initials: J
authors.lastname: Wu
authors.forename: Q
authors.initials: Q
authors.lastname: Min
authors.forename: C
authors.initials: C
authors.lastname: Ouyang
authors.forename: M
authors.initials: M
authors.lastname: Zheng
authors.forename: S
authors.initials: S
authors.lastname: Ma
authors.forename: W
authors.initials: W
authors.lastname: Yu
authors.forename: F
authors.initials: F
authors.lastname: Lin
mesh_terms: D000818:Animals; D044946:Biflavonoids / Q000494:pharmacology*; D001921:Brain / Q000201:enzymology / Q000473:pathology; D002545:Brain Ischemia / Q000201:enzymology / Q000378:metabolism*; D002392:Catechin / Q000494:pharmacology*; D002457:Cell Extracts; D002544:Cerebral Infarction / Q000201:enzymology / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D005707:Gallic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D005979:Glutathione Peroxidase / Q000378:metabolism; D020672:I-kappa B Proteins / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008315:Malondialdehyde / Q000378:metabolism; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000378:metabolism*; D009422:Nervous System Diseases / Q000473:pathology; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D015427:Reperfusion Injury / Q000201:enzymology / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D044946:Biflavonoids; D002457:Cell Extracts; D020672:I-kappa B Proteins; D016328:NF-kappa B; C000606206:Nfkbia protein, rat; D000072000:NF-KappaB Inhibitor alpha; C088983:theaflavine gallate; D009569:Nitric Oxide; D008315:Malondialdehyde; D005707:Gallic Acid; D002392:Catechin; D005979:Glutathione Peroxidase; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; D013482:Superoxide Dismutase