Epigallocatechin gallate attenuates amyloid β-induced inflammation and neurotoxicity in EOC 13.31 microglia

Microglia are the primary immune cells that contribute to neuroinflammation by releasing various proinflammatory cytokines and neurotoxins in the brain. Microglia-mediated neuroinflammation is one of the key characteristics of Alzheimer's disease (AD). Therefore, inhibitory reagents that prevent microglial activation may be used as potential therapeutic agents for treating AD. Recently, many studies have been performed to determine the bioactivities of green tea polyphenol epigallocatechin-3-gallate (EGCG), an efficient antioxidant that prevents neuroinflammation. However, limited information is available on the effects of EGCG on microglia-mediated neuroinflammation. In this study, we investigated the inhibitory effects of EGCG on amyloid beta (A beta)-induced microglial activation and neurotoxicity. Our results indicated that EGCG significantly suppressed the expression of tumor necrosis factor alpha (TNF alpha), interleukin-1 beta, interleukin-6, and inducible nitric oxide synthase (iNOS) in A beta-stimulated EOC 13.31 microglia. EGCG also restored the levels of intracellular antioxidants nuclear erythroid-2 related factor 2 (Nrf2) and heme oxygenase-1 (HO-1), thus inhibiting reactive oxygen species-induced nuclear factor-kappa B (NF-kappa B) activation after A beta treatment. Furthermore, EGCG effectively protected neuro-2a neuronal cells from A beta-mediated, microglia-induced cytotoxicity by inhibiting mitogen-activated protein kinase-dependent, AP-induced release of TNF alpha. Taken together, our findings suggested that EGCG suppressed A beta-induced neuroinflammatory response of microglia and protected against indirect neurotoxicity. These results suggest that EGCG is a possible therapeutic agent for preventing A beta-induced inflammatory neurodegeneration. (C) 2015 Elsevier B.V. All rights reserved.