Objective:To study the effect of inhibiting nuclear transcription factor- kappa B (NF-κB) on expression of chemokines in renal tubular epithelial cells induced by tumor necrosis factor (TNF)-α combined with interferon (IFN)-γ and the mechanism of 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) of peroxisome proliferator activated receptor-gamma (PPAR-γ) inhibits the expression of chemokines. Methods:HK-2 cells were divided into four groups:the control group,the TNF-α plus with IFN-γ treatment group,the pyrrolidine dithiocarbamate (PDTC) treatment group and the 15d-PGJ2 treatment group. The expressions of CXCL9,CXCL10 and CXCL11 mRNA were measured by real-time quantitative PCR and the levels of CXCL9,CXCL10 and CXCL11 in culture supernatant were examined by ELISA. The expressions of p65,IκB-α and p-p65,and p-IκBα were measured by Western blotting assay. Results:The mRNA expression and protein secretion of CXCL9,CXCL10 and CXCL11 in HK-2 cells were up-regulated after TNF-α and IFN-γ stimulation (P < 0.05). CXCL9,CXCL10 and CXCL11 were down-regulated by 85.44%,45.94% and 45.03% at mRNA level (P < 0.05) and 60.87%,47.59% and 53.42% at protein level (P < 0.05) when pretreated with PDTC;when pretreated with 15d-PGJ2,CXCL9,CXCL10 and CXCL11 were down-regulated by 93.87%,92.4% and 86.81% at mRNA level (P < 0.01) and 60.87%,47.59% and 53.42% at protein level (P < 0.01),and Western blot results showed that the phosphorylation levels of p65 and IκBα were down-regulated (P < 0.01). Conclusion:Inhibition of NF-κB decreases the expression of CXCL9,CXCL10 and CXCL11. The expressions of CXCL9,CXCL10 and CXCL11 could be inhibited by 15d-PGJ2 through the NF-κB signal pathway.