Objective To explore the molecular mechanism of emodin inhibiting orbital fibroblast fibrosis in Graves oph-thalmopathy.Methods The primary fibroblasts were isolated from orbital adipose connective tissue of patients with Graves oph-thalmopathy by collagenase digestion,the drug toxicity of emodin on fibroblasts was detected by MTT method,the effect of emodin on the migration ability of cells treated with TGF-β was detected by scratch test,and the expression of fiber related markers(CT-GF,fibronectin,collagen Ⅰ,α-SMA)and JNK,P38 of emodin on TGF-β treated cells was detected by immunoblotting.The activity of MMP2/MMP9 enzyme in the supernatant of cells treated with emodin TGF-β was detected by fluorescence ELISA.Results Low concentration emodin had no cytotoxicity to primary fibroblasts,and effectively inhibited TGF-β-induced cell migration and the expression of fibrosis-related markers,as well as the expression and enzyme activity of MMP2 and MMP9.It was further found that emodin inhibited the phosphorylation of P38 and JNK induced by TGF-β.Conclusion Emodin inhibits TGF-β-induced orbital fi-broblast fibrosis by regulating P38 and JNK signal pathways in Graves ophthalmopathy.
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