Effect of lipopolysaccharide of Porphyromonas gingivalis on prostaglandin E2 biosynthetic pathway in human monocytic cell strain THP-1
10.3321/j.issn:1002-0098.2008.08.010
- VernacularTitle:牙龈卟啉单胞菌脂多糖对人单核细胞株THP-1前列腺素E2合成通路的影响
- Author:
Yan-Min WU
1
;
Li-Li CHEN
;
Wei-Lian SUN
;
Jie YAN
Author Information
1. 浙江大学医学院附属第二医院
- Keywords:
Porphyromonas gingivalis;
Lipopolysaccharides;
Dinoprostone;
Prostaglandin Esynthase
- From:
Chinese Journal of Stomatology
2008;43(8):483-487
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of lipopolysaccharide of Porphyromonas gingivalis (Pg-LPS) on the bio-thythetic pathway of prostaglandin E2 (PGE2) and its difference from lipopolysaccharide of Escherichia coli (Ec-LPS). Methods Purified Pg-LPS and Ec-LPS were used to stimulate a humanm onocytic cell strain THP-1. PGE2 concentration was determined by an enzyme immunoassay kit. The release of tritium labeled arachidonic acid (AA) was detected by a liquid scintillation counter. Reverse transcription polymerase chain reaction and western blot were used to analyse the expression of cytosolic phospholipase A2 (cPLA2) enzyme, cyclooxygcnase-2 (COX-2), and mierosomal prostaglandin E synthase-1 (mPGES-1).Results The effect of Pg-LPS on induction of PGE2 and release of AA was significantly weaker than that of Ec-LPS (P <0. 05). Increased secretion of PGE2 was observed after stimulation with Pg-LPS for 6 h, which peak at 24 h at (221.40±29.46) ng/L; or with Ec-LPS for 1-48 h ,at (161.80±17.31) - (379.80±37. 35) ng/L. The highest levels of COX-2 and mPGES-1 were shown after 16 h treatment by Pg-LPS, or after 8 h and 16 h by Ec-LPS respectively, cPLA2 inhibitor AACOCF3 canht lower the level of LPS-induced release of AA, while it did not influence the production of PGE2 COX-2 inhibitor NS-398 could remarkably reduce the concentration of PGE2. Conclusions Pg-LPS showed delayed and weaker effect on PGE2 biosynthetic pathway thanEc-LPS. Pg-LPS-induced PGE2 synthesis was mainly due to enhanced expression of COX-2 and mPGES-1, whereas cPLA2 played an insignificant role.