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Neuronal Death and Apoptosis

開催日 2014/9/13
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

LPS-induced nitric oxide production is mediated by down-regulation of Pls synthesis in microglial cell line

  • P3-085
  • サレアハマド ヨセフ モハメド / Mohammed Youssef Saleh Ahmed:1 ホセイン M シャミン / Shamim M Hossain:1 三明 清隆 / Kiyotaka Miake:2 イブラハム アハマド / Ahmed Ibrahim:3 片渕 俊彦 / Toshihiko Katafuchi:1 
  • 1:九大・医・統合生理 / Dept Integr Physiol Kyushu Univ Grad Sch Med Sci 2:丸大食品㈱中央研究所 / Center Research Institute, Marudai Food. Co. 3:Dept Animal Physiol, Fac Vet Med, South Valley Univ, Qena, Egypt Dept Poultry Diseases, Fac Vet Med, South V / Dept Animal Physiol, Fac Vet Med, South Valley Univ, Qena, Egypt Dept Poultry Diseases, Fac Vet Med, South Valley Univ, Qena, Egypt 

The inflammatory responses associated with brain infection and neurodegenerative diseases are accompanied by production of high level of pro-inflammatory cytokines and oxidative stresses exerted against neurons. Brain microglia is one of the major players of the brain inflammatory responses by reacting to, for example, an endotoxin, lipopolysaccharides (LPS) through toll like receptor 4 (TLR4). Excessive response of microglia is risky for neurons because of high levels of oxygen and nitrogen radicals. Recently, one of the ether type glycerophospholipids, plasmalogens (Pls), were found to have an ameliorative impact against inflammatory cytotoxic effect of LPS; e.g., the decrease in the LPS-induced accumulation of ß-amyloid protein in neurons and the suppression of the LPS-induced activations of microglia. In this study we tried to investigate if Pls can affect nitric oxide (NO) production pathway in microglial cell line (MG6) and the relationship between Pls biosynthesis and LPS. Consequently we found that Pls succeeded to decrease the level of LPS-induced NO production from MG6 cells. Moreover the knockdown of endogenous Pls synthesizing enzymes, Glyceronphosphate O-Acyltransferase (GNPAT) and Alkyl-Glyceronphosphate synthase (AGPS), in MG6 cells revealed an enhanced NO production which was recovered by addition of Pls. Interestingly LPS suppressed the expression of GNPAT and AGPS. In addition we found that both NO production and AGPS-GNPAT down-regulation is regulated by P38-MAPK and c-Jun N-terminal kinase (JNK) related mechanisms. The present findings suggest that LPS-induced NO production is at least partly mediated by down-regulation of Pls synthesizing enzymes. Further studies are needed to elucidate the mechanisms of Pls actions.

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