| First Author | Lee YK | Year | 2009 |
| Journal | Brain Res | Volume | 1250 |
| Pages | 164-74 | PubMed ID | 18992719 |
| Mgi Jnum | J:147816 | Mgi Id | MGI:3842251 |
| Doi | 10.1016/j.brainres.2008.10.012 | Citation | Lee YK, et al. (2009) (-)-Epigallocatechin-3-gallate prevents lipopolysaccharide-induced elevation of beta-amyloid generation and memory deficiency. Brain Res 1250:164-74 |
| abstractText | Neuroinflammation has been known to play a role in the pathogenesis of AD. Our previous study showed that lipopolysaccharide (LPS) induced memory impairment through the accumulation of Abeta via the increase of beta- and gamma-secretase. In this study, we investigated the possible preventive effect of (-)-epigallocatechin-3-gallate (EGCG) on memory deficiency caused by LPS through the inhibition of Abeta(1-42) generation. Oral treatment with EGCG (1.5 and 3 mg/kg, for 3 weeks) into drinking water ameliorated LPS (1 microg/mouse, i.c.v.)-induced memory deficiency in a dose dependent manner. In addition, EGCG also dose-dependently inhibited LPS-induced elevation of Abeta level through attenuation of LPS-induced beta- and gamma-secretase activities and expression of its metabolic products; C99 and Abeta. Moreover, EGCG prevented LPS-induced neuronal cell death as well as the expression of inflammatory proteins, inducible nitric oxide synthetase and cyclooxygenase-2. This study therefore suggests that EGCG prevents LPS-mediated apoptotic cell death through the inhibition of the elevation of Abeta via the inhibition of beta- and gamma-secretases, and thus EGCG can be a useful agent against neuroinflammation-associated development or progression of AD. |
