Anti-inflammatory effects of glutamine on LPS-stimulated human dental pulp cells correlate with activation of MKP-1 and attenuation of the MAPK and NF-κB pathways

Aim To evaluate the anti‐inflammatory effects of glutamine and the underlying signal pathway mechanisms in lipopolysaccharide (LPS)‐stimulated human dental pulp cells (HDPCs). Methods Human dental pulp cells were exposed to 10 μg mL−1 LPS and various concentrations of glutamine for 24 h. The product...

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Veröffentlicht in:International endodontic journal 2015-03, Vol.48 (3), p.220-228
Hauptverfasser: Kim, D.-S., Shin, M.-R., Kim, Y.-S., Bae, W.-J., Roh, D.-H., Hwang, Y.-S., Kim, E.-C.
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Sprache:eng
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Zusammenfassung:Aim To evaluate the anti‐inflammatory effects of glutamine and the underlying signal pathway mechanisms in lipopolysaccharide (LPS)‐stimulated human dental pulp cells (HDPCs). Methods Human dental pulp cells were exposed to 10 μg mL−1 LPS and various concentrations of glutamine for 24 h. The production of PGE2 and nitric oxide was determined by enzyme‐linked immunosorbent assay (ELISA) and Griess reagent kit, respectively. Cytokines were examined by ELISA, reverse transcriptase‐polymerase chain reaction (RT‐PCR) and real‐time PCR. iNOS and COX protein expression as well as signal pathways were accessed by Western blot. The data were analysed by anova with Bonferroni's test (α = 0.05). Results Glutamine reduced LPS‐induced iNOS and COX‐2 protein expression as well as production of NO and PGE2 in a dose‐dependent fashion. Additionally, glutamine suppressed the production and mRNA expression of inflammatory cytokines including interleukin‐1β (IL‐1β), TNF‐α, and IL‐8. Furthermore, glutamine attenuated phosphorylation of extracellular signal‐regulated kinase (ERK), p38, c‐Jun N‐terminal kinase (JNK) and IκB‐α, and nuclear translocation of NF‐kB p65, but enhanced mitogen‐activated protein kinase phosphatase‐1 (MKP‐1) expression in LPS‐treated HDPCs. Conclusion Glutamine exerted an anti‐inflammatory effect via activation of MKP‐1 and inhibition of the NF‐kB and MAPK pathways in LPS‐treated HDPCs.
ISSN:0143-2885
1365-2591
DOI:10.1111/iej.12303