title: Sauchinone suppresses lipopolysaccharide-induced inflammatory responses through Akt signaling in BV2 cells.
abstract: Activated microglial cells play an important role in inflammatory responses in the central nervous system (CNS) that are involved in neurodegenerative diseases. Sauchinone has been shown to modulate the expression of inflammatory factors through nuclear factor-kappa B (NF-κB) signaling pathway. Here, we examined the effect of sauchinone on the inflammatory responses of microglia cells induced by lipopolysaccharide (LPS) and explored the mechanism underlying action of sauchinone. BV2 cells treated with LPS showed an up-regulation of nitric oxide (NO) and prostaglandin (PGE(2)) release, whereas sauchinone suppressed this up-regulation. Sauchinone inhibited both mRNA and protein expression of COX-2, iNOS, TNF-α and IL-1β. In addition, sauchinone blocked the activation of NF-κB through its inhibition of I-κB phosphorylation. Interestingly, sauchinone had no effect on the LPS-induced phosphorylation of mitogen activated protein kinases (MAP kinases; ERK1/2, p38, JNK), but it did inhibit Akt phosphorylation. These results suggest that the inhibitory effect of sauchinone on the LPS-induced production of inflammatory mediator in BV2 cells is associated with the suppression of the NF-κB and Akt signaling pathways. Therefore, sauchinone may be a useful treatment for neurodegenerative disease by inhibiting inflammatory responses in activated microglia.
authors: Department of physiology, College of Oriental Medicine, Daegu Haany University, Daegu 706-828, South Korea.
authors: Eun Young
authors: EY
authors: Jang
authors: Chae Ha
authors: CH
authors: Yang
authors: Min Ho
authors: MH
authors: Han
authors: Yung Hyun
authors: YH
authors: Choi
authors: Meeyul
authors: M
authors: Hwang
mesh_terms: D000818:Animals; D001578:Benzopyrans / Q000494:pharmacology*; D002460:Cell Line; D015232:Dinoprostone / Q000378:metabolism; D004149:Dioxoles / Q000494:pharmacology*; D006801:Humans; D007165:Immunosuppression Therapy; D007249:Inflammation / Q000276:immunology*; D018836:Inflammation Mediators / Q000378:metabolism; D008070:Lipopolysaccharides / Q000276:immunology; D051379:Mice; D017628:Microglia / Q000187:drug effects* / Q000276:immunology; D016328:NF-kappa B / Q000378:metabolism; D019636:Neurodegenerative Diseases / Q000276:immunology*; D009569:Nitric Oxide / Q000378:metabolism; D051058:Oncogene Protein v-akt / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D001578:Benzopyrans; D004149:Dioxoles; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D016328:NF-kappa B; C410958:sauchinone; D009569:Nitric Oxide; D051058:Oncogene Protein v-akt; D015232:Dinoprostone