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. 2014 Apr 22;2014:818251. doi: 10.1155/2014/818251

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 (P > 0.05).
Location and qualitative expression of A3AR, NF-κB p65, IκB-α, and phosphorylated-IκB-α in HT-29 cells treated with TNF-α, and/or 2-Cl-IB-MECA TNF-α-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-α attenuated NF-κB p65 nuclear translocation and suppressed the phosphorylation of IκB-α.
mRNA and protein expression of A3AR in HT-29 cells treated with TNF-α and/or 2-Cl-IB-MECA The mRNA and protein expression of A3AR showed no significant change among the NC group, TNF-α-only treated group, and 2-Cl-IB-MECA + TNF-α groups (P > 0.05).
Effects of 2-Cl-IB-MECA on TNF-α-induced NF-κB activation Pretreatment with 2-Cl-IB-MECA prior to stimulation with TNF-α 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-α, and reduced phosphorylated-IκB-α level, compared to TNF-α-only-treated groups (P < 0.05)
Effects of 2-Cl-IB-MECA on TNF-α-induced IL-8 and IL-1β expression 2-Cl-IB-MECA significantly decreased TNF-α-stimulated IL-8 and IL-1β mRNA expression and secretion, compared to the TNF-α-only-treated group (P < 0.05)