Fig. 9
Nimodipine exerts anti-fibrotic effects by suppressing CaMKII/STAT1 signaling pathway in OFs. a Co-IP identified an interaction between STAT1 and CaMKII in TED-OFs, n = 3. b–d WB showed KN-93 phosphate pretreatment (10 μmol/L) for 1 h inhibited TGF-β1 induced p-CaMKII (Thr286/287) protein expression at 30 min and TGF-β1 induced p-STAT1(Ser727) protein expression at 2 h, in TED-OFs, n = 3. e–h WB showed fludarabine pretreatment (10 μmol/L) for 1 h suppressed TGF-β1 induced p-STAT1(Ser727) protein expression at 2 h and TGF-β1 induced α-SMA and Col1A1 protein expression at 48 h, in TED-OFs, n = 3. i–l WB showed that nimodipine pretreatment dose-dependently suppressed TGF-β1 induced p-STAT1 (Ser727) protein expression at 2 h and TGF-β1 induced α-SMA, Col1A1 protein expression at 48 h, in TED-OFs, n = 3. The significance was determined by unpaired Student’s t-test (c, d, f–h) or one-way ANOVA (j–l). *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant. CaMKII, Ca2+/calmodulin-dependent protein kinase II; STAT1, signal transducer and activator of transcription 1; OF, orbital fibroblast; Co-IP, co-immunoprecipitation; TED-OFs, OFs derived from patients with TED; WB, western blot analysis; TGF-β1, transforming growth factor-beta 1; α-SMA, alpha-smooth muscle actin; Col1A1, collagen type I alpha 1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; WCL, whole cell lysate; Flu, fludarabine; Nimo, nimodipine