Open AccessAnti-inflammatory effects of egg white combined with chalcanthite in lipopolysaccharide-stimulated BV2 microglia through the inhibition of NF-κB, MAPK and PI3K/Akt signaling pathways
Author(s) -
Eun A Choi,
Hye Young Park,
HwaSeung Yoo,
Yung Hyun Choi
Publication year - 2012
Publication title -
international journal of molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.048
H-Index - 90
eISSN - 1791-244X
pISSN - 1107-3756
DOI - 10.3892/ijmm.2012.1169
Subject(s) - protein kinase b , pi3k/akt/mtor pathway , mapk/erk pathway , nf κb , nitric oxide , signal transduction , chemistry , tumor necrosis factor alpha , p38 mitogen activated protein kinases , kinase , iκbα , microglia , nitric oxide synthase , microbiology and biotechnology , pharmacology , biology , biochemistry , inflammation , endocrinology , immunology
Egg white-chalcanthite (EWCC) is a mixture of egg white and chalcanthiteprepared by roasting chalcanthite (which is a natural mineral mainly composedof CuSO4•5H2O) to the point of dehydration, pulverizing the dehydrated chalcanthiteand then mixing the pulverized chalcanthite to react with egg white to triggera reaction. When egg white-chalcanthite is prepared in this manner, the toxicityof chalcanthite is neutralized by the egg white, so that the toxicity is reducedor removed and the pharmaceutical properties are increased. However, the cellularand molecular mechanisms underlying the pharmacological activity of EWCC remainpoorly understood. In this study, we investigated the inhibitory effects of EWCCon the production of lipopolysaccharide (LPS)-induced pro-inflammatory mediatorsin BV2 microglia. Our data indicated that the EWCC treatment significantly inhibitedthe excessive production of nitric oxide and prostaglandin E2 in LPS-stimulatedBV2 microglia in a concentration-dependent manner without causing cytotoxicity.It also attenuated the expression of inducible nitric oxide synthase, cyclooxygenase-2and pro-inflammatory cytokines, including interleukin-1β and tumor necrosis factor-α.Moreover, EWCC exhibited anti-inflammatory properties by the suppression of nuclearfactor‑κB (NF-κB) activation by blocking IκB-α degradation, downregulation ofextracellular signal-regulated kinase, c-Jun N-terminal kinase, p38 mitogen-activatedprotein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/Akt pathways. Our resultsindicate that the inhibitory effects of EWCC on LPS-stimulated inflammatory mediatorproduction in BV2 microglia are associated with the suppression of the NF-κB,MAPK and PI3K/Akt signaling pathways. These findings suggest that EWCC may offera substantial therapeutic potential for the treatment of neurodegenerative diseasesthat are accompanied by microglial activation.