罗格列酮缓解皮损性硬皮病成纤维细胞的持续纤维化表型。
Rosiglitazone alleviates the persistent fibrotic phenotype of lesional skin scleroderma fibroblasts.
机构信息
Centre for Rheumatology, University College London (Royal Free Campus), London, UK.
出版信息
Rheumatology (Oxford). 2010 Feb;49(2):259-63. doi: 10.1093/rheumatology/kep371. Epub 2009 Dec 9.
OBJECTIVE
The transcription factor peroxisome proliferator-activated receptor (PPAR)-gamma plays an important role in controlling cell differentiation. The aim of the present study was to examine whether PPAR-gamma expression was reduced in skin scleroderma fibroblasts and whether PPAR-gamma agonists could suppress the persistent fibrotic phenotype of skin scleroderma fibroblasts.
METHODS
Dermal fibroblasts were isolated from site-, age- and sex-matched healthy individuals and lesional areas of individuals with dcSSc. Western blot and collagen gel contraction analyses were used to detect protein expression in the presence or absence of the PPAR-gamma agonist rosiglitazone.
RESULTS
PPAR-gamma expression was reduced in dcSSc fibroblasts. The PPAR-gamma agonist rosiglitazone alleviated the persistent fibrotic phenotype of dcSSc fibroblasts.
CONCLUSION
Rosiglitazone may alleviate the extent of fibrosis in dcSSc.
目的
转录因子过氧化物酶体增殖物激活受体（PPAR）-γ在控制细胞分化方面发挥着重要作用。本研究旨在检测皮肤硬皮病成纤维细胞中 PPAR-γ表达是否降低，以及 PPAR-γ激动剂是否可以抑制皮肤硬皮病成纤维细胞持续的纤维化表型。
方法
从年龄、性别和部位匹配的健康个体的皮肤和 dcSSc 个体的皮损区分离真皮成纤维细胞。存在或不存在 PPAR-γ激动剂罗格列酮的情况下，通过 Western blot 和胶原凝胶收缩分析检测蛋白表达。
结果
dcSSc 成纤维细胞中 PPAR-γ表达降低。PPAR-γ激动剂罗格列酮减轻了 dcSSc 成纤维细胞持续的纤维化表型。
结论
罗格列酮可能减轻 dcSSc 的纤维化程度。
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