Modulation of the Oxidative Stress and Nuclear Factor Kappa B Activation by Theaflavin 3,3'-gallate in the Rats Exposed to Cerebral Ischemia-Reperfusion

• Published in: Folia biologica Vol. 53; no. 5; pp. 164 - 172
• Main Authors: Cai, F, Li, C, Wu, J, Min, Q, Ouyang, C, Zheng, M, Ma, S, Yu, W, Lin, F
• Format: Journal Article
• Language: English
• Published: 01.01.2007
• ISSN: 0015-5500

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