[PPAR-γ agonist inhibits the expressions of chemokines induced by IFN-γ and TNF-α in renal tubular epithelial cells].
Yanfang Song, Qing Lin, Jian Zheng, Xianjin Zhu, Shunliang Yang
Abstract
Yanfang Song, Qing Lin, Jian Zheng, Xianjin Zhu, Shunliang Yang
Abstract
OBJECTIVE: To investigate the effect of peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist 15d-PGJ2 on the expressions of CXCL9, CXCL10 and CXCL11 in renal tubular epithelial cells (HK-2) stimulated by interferon-γ (IFN-γ) plus tumor necrosis factor-α (TNF-α). METHODS: HK-2 cells were stimulated with IFN-γ plus TNF-α only, or incubated with 15d-PGJ2 for 48 hours. CXCL9, CXCL10 and CXCL11 expressions were determined by real-time quantitative PCR (qRT-PCR) and ELISA. RESULTS: IFN-γ plus TNF-α increased mRNA and protein expressions of CXCL9, CXCL10 and CXCL11 in HK-2 cells. PPAR-γ agonist 15d-PGJ2 inhibited the expressions of CXCL9, CXCL10 and CXCL11 in IFN-γ combined with TNF-α-induced HK-2 cells. Compared with the IFN-γ plus TNF-α group (untreated with 15d-PGJ2), the CXCL9, CXCL10 and CXCL11 were depressed by 76.8%, 78.7% and 81.9% at mRNA level and 66.9%, 86.6% and 39.9% at protein level in 2.0 ng/mL 15d-PGJ2-treated HK-2 cells, respectively (P<0.05). CONCLUSION: PPAR-γ agonist 15d-PGJ2 could inhibit CXCL9, CXCL10 and CXCL11 production induced by IFN-γ combined with TNF-α in HK-2 cells.
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OBJECTIVE: To investigate the effect of peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist 15d-PGJ2 on the expressions of CXCL9, CXCL10 and CXCL11 in renal tubular epithelial cells (HK-2) stimulated by interferon-γ (IFN-γ) plus tumor necrosis factor-α (TNF-α). METHODS: HK-2 cells were stimulated with IFN-γ plus TNF-α only, or incubated with 15d-PGJ2 for 48 hours. CXCL9, CXCL10 and CXCL11 expressions were determined by real-time quantitative PCR (qRT-PCR) and ELISA. RESULTS: IFN-γ plus TNF-α increased mRNA and protein expressions of CXCL9, CXCL10 and CXCL11 in HK-2 cells. PPAR-γ agonist 15d-PGJ2 inhibited the expressions of CXCL9, CXCL10 and CXCL11 in IFN-γ combined with TNF-α-induced HK-2 cells. Compared with the IFN-γ plus TNF-α group (untreated with 15d-PGJ2), the CXCL9, CXCL10 and CXCL11 were depressed by 76.8%, 78.7% and 81.9% at mRNA level and 66.9%, 86.6% and 39.9% at protein level in 2.0 ng/mL 15d-PGJ2-treated HK-2 cells, respectively (P<0.05). CONCLUSION: PPAR-γ agonist 15d-PGJ2 could inhibit CXCL9, CXCL10 and CXCL11 production induced by IFN-γ combined with TNF-α in HK-2 cells.
Key concepts: CXCL10, CXCL11, Tumor necrosis factor alpha, Agonist, CXCL9, Chemokine, Chemistry, Receptor