2005 Volume 98 Issue 1 Pages 16-24
Extracts of Chinese herbs have been demonstrated to inhibit oxidative stress in vitro. In this study, we investigated the mechanism of (+)-catechin, isolated from green tea, which preserved murine microglia N9 cells from an oxidative agent tert-butylhydroperoxide (tBHP)-induced cell death. (+)-Catechin augmented the cell survival ratio after exposure to tBHP. Protective action of this drug was more efficacious than that of N-acetylcysteine, which is a putative antioxidant. DNA damage, detected by the Comet assay, was diminished with treatment of the drug. Results of flow cytometric analysis showed that the amount of intracellular · OH was decreased, and the cell cycle arrest was reversed by down-regulation of p53 phosphorylation after treatment with (+)-catechin. The reduced p53 activity followed the impairment of NF-κB translocation to the nuclear region. Then the phosphorylation of extracellular signal regulated protein kinase, a cell survival facilitative signal, was upregulated at the later stage. Taken together, (+)-catechin inhibited tBHP-induced translocation of NF-κB to improve cellular survival.