Pirfenidone suppresses the abnormal activation of human Müller cells after platelet-derived growth factor-BB stimulation
Pirfenidone suppresses the abnormal activation of human Müller cells after platelet-derived growth factor-BB stimulation作者机构：Department of Ophthalmologythe First Affiliated Hospital of Kunming Medical University Kunming 650031Yunnan Province China Department of Ophthalmologythe First Affiliated Hospital of Nanjing Medical University Nanjing 210029Jiangsu ProvinceChina
出 版 物：《International Journal of Ophthalmology(English edition)》 (国际眼科杂志（英文版）)
年 卷 期：2019年第12卷第7期
页 面：1075-1082页
核心收录：
主 题：pirfenidone Müller cells platelet-derived growth factor-BB transforming growth factor-β proliferative vitreoretinopathy
摘 要：AIM: To determine the effect of pirfenidone on the activated human Müller cells by platelet-derived growth factor-BB(PDGF-BB). METHODS: The primary human Müller cells were separated from retinal tissues and established the pathogenic model by stimulated with PDGF-BB. The Müller cells behaviour of normal group and the model group was measured by MTT assay, Trypan blue assay, cell migration assay, and collagen contraction assay. The expression of transforming growth factor(TGF)-β1,-β2, and pigment epithelium-derived factor(PEDF) was estimated with realtime polymerase chain reaction(PCR), Western blot and immunofluorescence analyses. RESULTS: A pathogenic/proliferative model of Müller cells was established by stimulating normal cultured Müller cells with 10 ng/mL PDGF-BB for 48 h. After treated with 0.2 and 0.3 mg/mL pirfenidone, the proliferation, migration and collagen contraction was statistically significantly depressed in the model group compared with the normal groups. The expression levels of TGF-β1 and TGF-β2 were significantly down-regulated, while the PEDF expression was significantly up-regulated after treated with 0.2 and 0.3 mg/mL pirfenidone in the model group. CONCLUSION: Pirfenidone effectively suppress the proliferation, migration and collagen contraction of the human Müller cells stimulated with PDGF-BB through down-regulation of TGF-β1/TGF-β2 and up-regulation of PEDF.
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