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Pirfenidone suppresses the abnormal activation of human Müller cells after platelet-derived growth factor-bb stimulation

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International Journal of Ophthalmology(English edition) 2019年第7期12卷 1075-1082页

作者： Yi-Jin Tao Qin Chen Li Wang Xiao Yang Qing Cun Wen-Yan Yang Hua Zhong Department of Ophthalmology the First Affiliated Hospital of Kunming Medical University Kunming 650031Yunnan Province China Department of Ophthalmology the First Affiliated Hospital of Nanjing Medical University Nanjing 210029Jiangsu ProvinceChina

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.

关键词： pirfenidone Müller cells platelet-derived growth factor-bb transforming growth factor-β proliferative vitreoretinopathy

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