Fig. 6

S1PR2 is the predominant S1PR expressed in macrophages and mediates NF-κB activation in macrophages. mRNA expression of S1PRs in primary peritoneal macrophages and RAW264.7 cells (A, B); S1PR2 and NF-κB p65 levels in RAW264.7 cells stimulated by different times and doses of TCA (C, D); Immunofluorescence staining of NF-κB in RAW264.7 cells (E); NF-κB levels in 266-6 cells, preincubated with or without JTE-013 and stimulated with TCA (100 µM) for 4 h (F); S1PR2 and NF-κB levels in adenovirus control and Ad-S1PR2–transduced RAW264.7 cells stimulated with TCA (100 µM) for 4 h (G); NF-κB levels in RAW264.7 cells, preincubated with or without JTE-013, Y27632, U0126, SB203590, and stimulated with TCA (100 µM) for 4 h (H); RAW264.7 cells were cultured in transwell inserts, and stimulated with JTE-013 for 30 min and then treated with TCA (100 µM) for 24 h (I); The mRNA levels of inflammatory factors in RAW264.7 cells stimulated with TCA (100 µM) for 4 h with or without JTE-013 (J). Data shown are means ± SEM. ***p < 0.001 compared with the control group. #p < 0.01, ###p < 0.001 compared with the TCA-treatment alone