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BTB and CNC homology 1 inhibition ameliorates fibrosis and inflammation via blocking ERK pathway in pulmonary fibrosis by Yuan Liu; Yongfu Wang; Fuai Lu; Le Wang; Liu Miao; Xiaoyuan Wang is a Medicine article available to read on EtoBox.

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## Objective: Patients with idiopathic pulmonary fibrosis (ipf) are still suffering from unfavorable survival. btb and cnc homology1 (bach1) is a regulator of oxidative stress and participates in the pathogenesis of multiple lung diseases. thus, this study aimed to determine the effect of bach1 knockdown on fibrosis and inflammation in pulmonary fibrosis (pf) mice and cell models. ## Methods: Bleomycin induced pf mice were constructed and treated with bach1 sirna adenovirus (blm + bach1 sirna group), control sirna adenovirus (blm + control sirna group) or normal saline (blm group), then lung tissues were collected for bach1 expression detection, h&e staining and masson's trichrome staining. afterwards, collagen type i alpha 1 chain (col1a1) and interleukin-6 (il-6) expressions in serum and bronchoalveolar lavage fluid (balf) were examined. subsequently, mouse lung fibroblasts (mlfs) were collected from pf mice and treated with tgf-β1 to construct pf cell model, which was treated with bach1 sirna adenovirus (tgf-β1 + bach1 sirna group) and map kinase (erk) inhibitor u0126 alone (tgf-β1 + u0126 group) or in combination (tgf-β1 + u0126 + bach1 sirna group), then alpha-smooth muscle ac

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Author

Yuan Liu; Yongfu Wang; Fuai Lu; Le Wang; Liu Miao; Xiaoyuan Wang

Publisher

Informa plc; Informa UK (Taylor & Francis); Taylor & Francis; Informa UK Limited (ISSN 0190-2148)

Published

2020

Language

EN

Field

Medicine (Health Sciences)