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Figure 4 | Journal of Inflammation

Figure 4

From: Interleukin-1β regulates the expression of glucocorticoid receptor isoforms in nasal polyps in vitro via p38 MAPK and JNK signal transduction pathways

Figure 4

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).

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