Extracellular CIRP Upregulates Proinflammatory Cytokine Expression via the NF-kappaB and ERK1/2 Signaling Pathways in Psoriatic Keratinocytes

Figure 5

C23 inhibited the eCIRP-induced upregulation of proinflammatory cytokine expression and activation of signaling pathways in M5-stimulated psoriatic keratinocytes. (a) C23 inhibited TNF-α, IL-6, and IL-8 production in psoriatic keratinocytes stimulated with rhCIRP. Cells were stimulated with M5 for 24 hours, pretreated with 1 μg/ml C23 for 30 minutes, and then incubated with 1 μg/ml rhCIRP for 1 hour. RNA was extracted for analysis by qRT-PCR. (b) C23 inhibited the phosphorylation of NF-κB p65 and ERK1/2 in psoriatic keratinocytes stimulated with rhCIRP. Cells were stimulated with M5 for 24 hours, pretreated with 1 μg/ml C23 for 30 minutes, and then incubated with 1 μg/ml rhCIRP for 1 hour. Cells were lysed for western blot analysis of the indicated proteins. The phosphorylation of NF-κB p65 and ERK1/2 was analyzed by western blot analysis. Data are expressed as the . /group. , , and vs. control; ^#, ^##, and ^###.

(a)

(b)