Figure 3.

The IFN-γ-induced IP-10/CXCL10 level was attenuated by the benzylideneacetophenone derivative compound, JC3, in a dose-dependent manner without an influence on the viability of orbital fibroblasts from patients with TAO. (a) TAO and non-TAO cells were pretreated with JC3 at 5, 10 and 20 μM for 30 min and then treated with IFN-γ (10 ng ml⁻¹) for 24 h; the supernatant was then collected to measure IP-10/CXCL10 protein by ELISA. The IP-10/CXCL10 expression level in IFN-γ-treated group was arbitrarily assigned a value of 100, and the data are presented as percentage reductions (*P<0.05 vs each IFN-γ group; BD, below detection limit). (b) TAO cells were pretreated with either yakuchinone B or JC3 at 10 μM for 30 min. Following treatment with IFN-γ (10 ng ml⁻¹) for 24 h, IP-10/CXCL10 production was measured and analyzed as described in A (*P<0.05 vs each IFN-γ-treated group; **P<0.05 in JC3-treated group vs yakuchinone B-treated group). (c) Orbital fibroblasts of patients with TAO patients were treated with IFN-γ (10 ng ml⁻¹) in the presence or absence of 5, 10 of 20 μM JC3 for 24 h. After treatment, cell viability was evaluated as described in the Materials and Methods section. Results are expressed as mean±s.d. in relative O.D. units (compared with control); normalized values are shown.