CCK-8 decreases RSC-364 proliferation and p38 MAPK activation induced by TNF-? in rats
- VernacularTitle:CCK-8降低TNF-?诱导的大鼠RSC-364细胞增殖及p38 MAPK活性
- Author:
Jinrong XU
- Publication Type:Journal Article
- Keywords:
cholecystokinin-octapeptide;
tumor necrosis factor;
synoviocytes;
p38 MAPK;
rheumatoid arthritis
- From:
Basic & Clinical Medicine
2006;0(03):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effect of cholecystokinin-octapeptide(CCK-8) on the proliferation of fibroblast-like synovial cell line RSC-364 and p38 MAPK activity induced by TNF-? in rat.Methods The proliferation of RSC-364 cells was measured by monotetrazolium(MTT) colourmetric assay and the level of activation of p38 MAPK was deteced by Western blot.Results An increase in p38 MAPK phosphorylation was detected 5 min after TNF-?((50 ?g/L))addition,and reached a plateau at(15 min),finally returned to the basic level at(2 h).TNF-?(10,25,(50 ?g/L)) increased p38 MAPK phosphorylation in a dose dependent manner at 15 min.CCK-8((10~(-10))～(10~(-6)mol/L))could inhibit the proliferation and the level of phosphorylation of p38 MAPK in a dose dependent manner.Moreover the inhibitory effects were partly reversed by CCK-A receptor specific antagonist CR1409 or CCK-B receptor specific antagonist CR2945.SB203580 inhibited TNF-?-stimulated RSC-364 proliferation.Conclusion CCK-8 inhibited TNF-?-stimulated proliferation by decreasing p38 MAPK phosphorylation in RSC-364 cells,which was mediated through CCK-A receptor or CCK-B receptor.
