Activation of Adenosine A3 Receptor Alleviates TNF-α-Induced Inflammation through Inhibition of the NF-κB Signaling Pathway in Human Colonic Epithelial Cells
Table 2
Summary of the important results.
Items
Results
Cell viability
No significant effect on cell viability was observed at test concentrations of up to 400 nM ().
Location and qualitative expression of A3AR, NF-κB p65, IκB-, and phosphorylated-IκB- in HT-29 cells treated with TNF-, and/or 2-Cl-IB-MECA
TNF--stimulated cells pretreated with 2-Cl-IB-MECA showed no obvious change in A3AR expression. Pretreatment with 2-Cl-IB-MECA and subsequent stimulation with TNF- attenuated NF-κB p65 nuclear translocation and suppressed the phosphorylation of IκB-.
mRNA and protein expression of A3AR in HT-29 cells treated with TNF- and/or 2-Cl-IB-MECA
The mRNA and protein expression of A3AR showed no significant change among the NC group, TNF--only treated group, and 2-Cl-IB-MECA + TNF- groups ().
Effects of 2-Cl-IB-MECA on TNF--induced NF-κB activation
Pretreatment with 2-Cl-IB-MECA prior to stimulation with TNF- attenuated NF-κB p65 nuclear translocation as p65 protein decreased in the nucleus of cells and increased in the cytoplasm, inhibited the degradation of IκB-, and reduced phosphorylated-IκB- level, compared to TNF--only-treated groups ()
Effects of 2-Cl-IB-MECA on TNF--induced IL-8 and IL-1 expression
2-Cl-IB-MECA significantly decreased TNF--stimulated IL-8 and IL-1 mRNA expression and secretion, compared to the TNF--only-treated group ()