Modulation of the oxidative stress and nuclear factor kappaB activation by theaflavin 3,3'-gallate in the rats exposed to cerebral ischemia-reperfusion.

The major pathobiological mechanisms of IR injury include excitotoxicity, oxidative stress, and inflammation. TF 3 , 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 TF 3 and its mechanisms against cerebral IR injury in rats. TF 3 administration (10 and 20 mg.kg −1 ) ame- liorated the infarct volume. TF 3 also decreased the content of MDA and NO. TF 3 significantly increased the activity of SOD and GSH-Px, which were reduced by IR injury. Administration of TF 3 decreased mRNA and protein expression of COX-2 and iNOS. DNA binding and Western blotting revealed an increase in NF-κB activation and IκB depletion in IR brain tis- sue. Pretreatment with TF 3 markedly inhibited IR- induced increase in nuclear localization of NF-κB, and preserved IκB in the cytoplasm. The results show that TF 3 exerts protective effects against cerebral IR injury by reducing oxidative stress and modulating the NF-κB activation.