趋化素在特发性肺纤维化中的表达及保护作用

C Y Shen, G R Li, D Wei, W Wang, X S Yang, C Jiang, Y T Sheng, Z K Yang, X W Nie, J Y Chen
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引用次数: 0

摘要

目的:探讨趋化素在特发性肺纤维化(IPF)中的表达及其作用。方法:采用定量PCR和Western blotting检测IPF患者和对照组肺组织中趋化素mRNA和蛋白水平。采用酶联免疫吸附法分析临床血清趋化素水平。将分离培养的小鼠肺成纤维细胞分为对照组、TGF-β组、TGF-β+趋化素组和趋化素组。采用免疫荧光染色法观察α-平滑肌肌动蛋白(α-SMA)的表达。将C57BL/6小鼠随机分为对照组、博来霉素组、博来霉素+趋化素组和趋化素组。采用马松染色和免疫组化染色评价肺纤维化的严重程度。在体外和体内肺纤维化模型中分别采用定量PCR和免疫组化染色检测上皮细胞向间质转化(EMT)标志物的表达。结果:与对照组相比,IPF患者肺组织和血清中chemerin的表达均下调。免疫荧光结果显示,TGF-β单独作用于成纤维细胞后,α-SMA表达明显增强,而TGF-β和趋化素联合作用于成纤维细胞后,α-SMA表达水平与对照组相似。Masson染色显示博莱霉素诱导的肺纤维化模型构建成功,而趋化素处理部分减轻了肺组织的损伤。免疫组化染色显示,博来霉素组大鼠肺组织中chemerin的表达明显降低。定量PCR和免疫组化结果显示,趋化素在体外和体内均能减弱TGF-β和博来霉素诱导的EMT。结论:趋化素在IPF患者中表达降低。Chemerin可能通过调节EMT对IPF的发展起到保护作用,为IPF的临床治疗提供了新的思路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Expression and protective effect of chemerin in idiopathic pulmonary fibrosis].

Objective: To explore the expression and the role of chemerin in idiopathic pulmonary fibrosis (IPF). Methods: Quantitative PCR and Western blotting were used to determine the mRNA and protein levels of chemerin in lung tissues from IPF patients and the controls. Clinical serum level of chemerin was analyzed by enzyme-linked immunosorbent assay. The mouse lung fibroblasts isolated and cultured in vitro were divided into the control, TGF-β, TGF-β+chemerin and chemerin groups. Immunofluorescence staining was used to observe the expression of α-smooth muscle actin (α-SMA). C57BL/6 mice were randomly divided into the control, bleomycin, bleomycin+chemerin, and chemerin groups. Masson and immunohistochemical staining were performed to evaluate the severity of pulmonary fibrosis. Expression of epithelial to mesenchymal transition (EMT) markers was detected by quantitative PCR and immunohistochemical staining in the in vitro and in vivo models of pulmonary fibrosis, respectively. Results: Compared with the control group, the expression of chemerin was downregulated in both the lung tissue and the serum of IPF patients. Immunofluorescence showed that treatment of fibroblasts with TGF-β alone resulted in a robust expression of α-SMA, whereas treatment with TGF-β and chemerin together exhibited the similar expression levels of α-SMA as the control group. Masson staining indicated that the bleomycin-induced pulmonary fibrosis model was constructed successfully, while treatment of chemerin partially alleviated the damage of lung tissue. Immunohistochemical staining showed that the expression of chemerin in the lung tissue was significantly decreased in the bleomycin group. Quantitative PCR and immunohistochemistry showed that chemerin attenuated EMT induced by TGF-β and bleomycin both in vitro and in vivo. Conclusions: The expression of chemerin was reduced in patients with IPF. Chemerin may play a protective role in the development of IPF by regulating EMT, providing a new idea for the clinical treatment of IPF.

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