四川医学2024，Vol.45Issue(12)：1340-1344,5.DOI:10.16252/j.cnki.issn1004-0501-2024.12.008
大黄素抑制Graves眼病眼眶成纤维细胞纤维化的分子机制研究
Study on the Molecular Mechanism of Emodin Inhibiting Orbital Fibroblast Fibrosis in Graves'Ophthalmopathy
朱劲 1张晓 1钟宇玲 1陈宏 1林文劼1
作者信息
- 1. 成都医学院第二附属医院·核工业四一六医院眼科,四川成都 610000
- 折叠
摘要
Abstract
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.关键词
大黄素/Graves眼病/成纤维细胞/纤维化Key words
emodin/Graves'ophthalmopathy/fibroblast/fibrosis分类
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朱劲,张晓,钟宇玲,陈宏,林文劼..大黄素抑制Graves眼病眼眶成纤维细胞纤维化的分子机制研究[J].四川医学,2024,45(12):1340-1344,5.
