(+)-Catechin, an ingredient of green tea, protects murine microglia from oxidative stress-induced DNA damage and cell cycle arrest

Abstract

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. © 2005 The Japanese Pharmacological Society.