Figure 4From: Interleukin-1β regulates the expression of glucocorticoid receptor isoforms in nasal polyps in vitro via p38 MAPK and JNK signal transduction pathways Involvement of p38 MAPK and JNK pathways in the regulation of GR isoform expression. A: Lane 1: Trace expressions of all target proteins in the control group; Lane 2: Increased expressions of all target proteins in the 20 ng/ml IL-1β group; Lane 3: JNK-specific inhibitor (SP600125) decreased the expressions of GR isoforms and phospho-JNK, but not that of phospho-p 38MAPK; Lane 4: P 38MAPK-specific inhibitor (SB203580) decreased the expressions of GR isoforms and phospho-p 38MAPK, but not that of phospho-JNK; Lane 5: Trace expressions of all target proteins were detected in nasal polyp tissue incubated with SB203580 or SP600125 but without IL-1β induction. Lane 6: SB203580 and SP600125 inhibited almost all expressions of GR isoforms, phospho-p 38MAPK and phospho-JNK in IL-1β-induced nasal polyp in vitro. Lane 7: Specific inhibitors (LY294002, PD98059 or Ro31-8220) of the PI3K, ERK or PKC pathways did not influence the expressions of GR isoforms, phospho-p 38MAPK and phospho-JNK in IL-1β-induced nasal polyp in vitro. B represents the densitometry value (Western blot bands in 4A) ratio of above-mentioned target proteins and β-actin. The protein levels shown are representative of three independent experiments with similar trend. (Western blot).Back to article page