Pirfenidone inhibits cell fibrosis in connective tissue disease-associated interstitial lung disease by targeting the TNF-α/STAT3/KL6 pathway

• DOI: 10.21037/jtd-22-41
• Publication Date: 2022-05-17T01:21:46Z
• Authors: Yanhua Zuo; Jing Liu; Huaheng Xu; Yanxia Li; Ran Tao; Zongfang Zhang
• Keywords: Pirfenidone; Vital capacity

To explore the effect and mechanism of pirfenidone in inhibiting pulmonary fibrosis connective tissue disease-associated interstitial lung disease (CTD-ILD).From 2018 to 2020, 50 CTD-ILD patients were enrolled clinical study. Based on whether was used during treatment, into group control group. Pulmonary function tests compared before after treatment. Enzyme-linked immunosorbent assay (ELISA) performed detect expression tumor necrosis factor-α (TNF-α), signal transducer activator transcription 3 (STAT3), Krebs Von den Lungen-6 (KL-6) venous blood Rat type II (RLE-6TN) epithelial cells cultivated for vitro experiments, they sorted group, bleomycin TNF-α Stattic TNF-α/Stattic combined treatment For 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) evaluate cell proliferation, Reverse Transcription-Polymerase Chain Reaction(RT-PCR) STAT3 KL-6 mRNA levels, ELISA utilized E-cadherin Western blotting (WB) determine α-smooth muscle actin (α-SMA), vimentin, TNF-α, STAT3, phosphorylated (PSTAT3) expression.In study, indices including forced expiratory volume one second (FEV1), vital capacity (FVC), FEV1/FVC, peak flow (PEF) partial pressure (PaO2) study superior those (P<0.05). The serum levels significantly lower than In α-SMA, Compared with TNF-α-treated upregulated Meanwhile, viability further (P<0.05), decreased Stattic-treated treated infliximab Stattic, increased activity restored inhibited (P<0.05).Pirfenidone improved 1 patients. Moreover, inhibits through TNF-α/STAT3/Mucin 1(MUC1) pathway.