Reference - Detail
|Author||Tsolmongyn B, Koide N, Odkhuu E, Haque A, Naiki Y, Komatsu T, Yoshida T, Yokochi T.|
|Title||Lipopolysaccharide prevents valproic acid-induced apoptosis via activation of nuclear factor-κB and inhibition of p53 activation.|
The effect of lipopolysaccharide (LPS) on valproic acid (VPA)-induced cell death was examined by using mouse RAW 264.7 macrophage cells. LPS inhibited the activation of caspase 3 and poly (ADP-ribose) polymerase and prevented VPA-induced apoptosis. LPS inhibited VPA-induced p53 activation and pifithrin-α as a p53 inhibitor as well as LPS prevented VPA-induced apoptosis. LPS abolished the increase of Bax/Bcl-2 ratio, which is a critical indicator of p53-mediated mitochondrial damage, in response to VPA. The nuclear factor (NF)-κB inhibitors, Bay 11-7082 and parthenolide, abolished the preventive action of LPS on VPA-induced apoptosis. A series of toll-like receptor ligands, Pam3CSK4, poly I:C, and CpG DNA as well as LPS prevented VPA-induced apoptosis. Taken together, LPS was suggested to prevent VPA-induced apoptosis via activation of anti-apoptotic NF-κB and inhibition of pro-apoptotic p53 activation. The detailed inhibitory mechanism of VPA-induced apoptosis by LPS is discussed.
|MeSH||Animals Apoptosis / drug effects* Cell Line Dose-Response Relationship, Drug Immunoblotting Lipopeptides / pharmacology Lipopolysaccharides / pharmacology* Macrophages / cytology Macrophages / drug effects Macrophages / metabolism Mice NF-kappa B / antagonists & inhibitors NF-kappa B / metabolism* Nitriles / pharmacology Oligodeoxyribonucleotides / pharmacology Poly I-C / pharmacology Proto-Oncogene Proteins c-bcl-2 / metabolism Sesquiterpenes / pharmacology Sulfones / pharmacology Toll-Like Receptor 9 / agonists Toll-Like Receptors / agonists Tumor Suppressor Protein p53 / metabolism* Valproic Acid / pharmacology* bcl-2-Associated X Protein / metabolism|
|WOS Category||IMMUNOLOGY CELL BIOLOGY|
|Human and Animal Cells|