Effects of cholecystokinin octapeptide on TNF-?-induced IL-6 expression and its possible molecular mechanism in rat synovial cell strain RSC-364
- VernacularTitle:八肽胆囊收缩素对TNF-?诱导的大鼠滑膜细胞株RSC-364 IL-6的作用及其可能的分子机制(英文)
- Author:
Zhansheng ZHAO
;
Yuhuai JIN
;
Bin CONG
;
Shujin LI
;
Jinrong XU
;
Yuxia YAO
;
Yiling LING
- Publication Type:Journal Article
- Keywords:
Arthritis,rheumatoid;
Cholecystokinin;
Synoviocytes;
Interleukin-6;
NF-kappa B
- From:
Chinese Journal of Pathophysiology
2000;0(07):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the effect of sulfated cholecystokinin octapeptide(CCK-8) on TNF-? induced IL-6 mRNA expression,NF-?B activation in the rat fibroblast-like synovial cell strain RSC-364 and its possible receptor mechanisms.METHODS:RSC-364 cells were stimulated with TNF-?(10 ?g/L) in the presence or absence of sCCK-8(10-8-10-6 mol/L) or/and CCK receptor antagonist proglumide(2 mg/L).IL-6 and CCK receptor A/B(CCK-AR/CCK/BR) mRNA expression were assayed by reverse transcription polymerase chain reaction(RT-PCR) at 3 h after stimulation,and nuclear factor-?B(NF-?B) binding activity was analyzed by electrophoretic mobility shift assay(EMSA) at 1h after stimulation.At 30 min of stimulation the I?B protein level in cytoplasma was measured by Western blotting.RESULTS:Both CCK-AR and CCK-BR were constitutively expressed on RSC-364.sCCK-8,at concentrations from 10-8 mol/L to 10-6 mol/L,significantly increased IL-6 mRNA expression,CCK-AR and CCK-BR mRNA expression,NF-?B binding activity and I?B protein degradation.The effects of sCCK-8 on NF-?B activity and I?B degradation level were attenuated by CCK receptor antagonist proglumide.CONCLUSION:sCCK-8 upregulats TNF-?-induced IL-6 mRNA expression by NF-?B pathway through its receptor on rat synoviocytes,suggesting its possible regulatory role in the pathogenesis of rheumatoid arthritis.
