Imrecoxib Inhibits Paraquat-Induced Pulmonary Fibrosis through the NF-κB/Snail Signaling Pathway.

Haihao Jin,Tao Huang

doi:10.1155/2020/6374014

Abstract

Objective In recent years, pulmonary fibrosis caused by paraquat poisoning is still concerned. However, no effective drugs have been developed yet to treat paraquat-induced pulmonary fibrosis. The aim of our research is to investigate whether imrecoxib can inhibit paraquat-induced pulmonary fibrosis and its possible mechanism. Methods Extraction of primary pulmonary fibrosis cells (PPF cells) in vitro by the method of trypsin digestion. RT-qPCR and western blot were employed to measure the transcription level and protein expression of EMT related markers in paraquat-induced A549 cells. MTT, wound-healing, and Transwell experiments were used to verify the effect of imrecoxib on the proliferation, migration, and invasion of PPF and HFL1 cells. Results Firstly, our results confirmed that paraquat can induce EMT and activate the NF-κB/snail signal pathway in lung epithelial cell A549. Furthermore, experimental results showed that imrecoxib could repress the proliferation, migration, and invasion of PPF and HFL1 cells. Finally, our study found that imrecoxib can inhibit EMT of paraquat-induced A549 cells by the NF-κB/snail signal pathway. Conclusion Imrecoxib can inhibit EMT of paraquat-induced A549 cells and alleviate paraquat-caused pulmonary fibrosis through the NF-κB/snail signal pathway. Therefore, imrecoxib is a drug worthy of study in the treatment of paraquat-induced pulmonary fibrosis.

Highlights

Human pulmonary fibrosis (PF), especially idiopathic pulmonary fibrosis (IPF), is a fatal and chronic disease that causes fibroblast proliferation and excessive deposition of relative protein, which in turn disrupts the lung structure and function and eventually leads to respiratory failure [1,2,3]
The RNA of two groups of A549 cells was extracted for the RT-qPCR assay, and the content of E-cadherin and vimentin in the two groups of A549 cells was determined by western blot
The data demonstrated that the expression of E-cadherin in the paraquat-induced group was much lower, but on the contrary, the expression of vimentin was significantly higher (Figures 1(a)–1(c)). These results indicated that paraquat can inhibit the expression of E-cadherin in A549 cells, while promote the vimentin expression, that is paraquat can induce the epithelial-mesenchymal transitions of A549 cells

Summary

Objective

Pulmonary fibrosis caused by paraquat poisoning is still concerned. no effective drugs have been developed yet to treat paraquat-induced pulmonary fibrosis. Extraction of primary pulmonary fibrosis cells (PPF cells) in vitro by the method of trypsin digestion. MTT, wound-healing, and Transwell experiments were used to verify the effect of imrecoxib on the proliferation, migration, and invasion of PPF and HFL1 cells. Our results confirmed that paraquat can induce EMT and activate the NF-κB/snail signal pathway in lung epithelial cell A549. Experimental results showed that imrecoxib could repress the proliferation, migration, and invasion of PPF and HFL1 cells. Our study found that imrecoxib can inhibit EMT of paraquat-induced A549 cells by the NF-κB/snail signal pathway. Imrecoxib can inhibit EMT of paraquat-induced A549 cells and alleviate paraquat-caused pulmonary fibrosis through the NF-κB/snail signal pathway. Imrecoxib is a drug worthy of study in the treatment of paraquat-induced pulmonary fibrosis

Introduction

Materials and Methods

Results

Discussion