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ISSN: 2167-7700

Chemotherapy: Open Access
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Short Article

Status of Stress and Cognitive of Cancer Patients with PICC Ultrasound Guidance Catheterization: A Questionnaire Survey

Xianglong Kong1, Hui Li1, Qi Hu1, Yusheng Yan1, Wenfang Tang1, Yuling Tang1#* and Zheyu Hu2#*

1Department of Respiration Medicine, The First Hospital of Changsha, PR China

2Department of Clinical Research and Teaching, The First Hospital of Changsha, PR China

#These authors contributed equally to this work

*Corresponding Authors:
Yuling Tang
Department of Respiration Medicine
The First Hospital of Changsha, PR China
Tel: +30 2103381845
E-mail: [email protected]
 
Zheyu Hu
Department of Clinical Research and Teaching
The First Hospital of Changsha, PR China
Tel: 86-731-8491-1120
E-mail: [email protected]

Received date: July 22, 2017; Accepted date: August 11, 2017; Published date: August 16, 2017

Citation: Kong X, Li H, Hu Q, Yan Y, Tang W, et al. (2017) Neferine Attenuates Epithelial-Mesenchymal Transition of Alveolar Epithelial Cells via TGF-β Signaling Pathway. Chemo Open Access 6: 241. doi:10.4172/2167-7700.1000241

Copyright: © 2017 Kong X, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Background: Idiopathic pulmonary fibrosis (IPF) is an incurable, progressive, and fatal interstitial lung disease with the characteristics of lung tissue damage and an enhancement in extracellular matrix (ECM). Alveolar epithelial cells (AMs) are major target cells that can directly promote to occurring of pulmonary fibrosis by acquisition of a mesenchymal phenotype through epithelial- mesenchymal transition (EMT). Neferine, a component of Chinese herbs, has been thought to be involved in anti-fibrotic activity in experimental lung fibrosis. However, its mechanism is not clear. In this study, we explore the regulation of neferine in TGF-β-induced EMT in lung fibrosis model and illustrate its mechanism of action.

Methods: The alveolar epithelial cell line A549 was stimulated with TGF-β1 with or without Neferine pretreatment in advance. Morphologic variations and expression of EMT-related markers, including E-cadherin, β-catenina-SMA and Vimentin were detected. Expressions of Smad2, p- Smad 2, Smad3 and p-Smad3 were measured.

Results: TGF-β1–treated A549 cells were transformed into the mesenchymal morphology with less E-cadherin, β-catenin and more a-SMA, Vimentin expression. The addition of Neferine inhibited the TGF-β1–induced change of the mesenchymal phenotype. Furthermore, Neferine inhibited the TGF-β1–induced increase in the expression of p- Smad2 and p-Smad3.

Conclusions: Our study illustrate that Neferine inhibits TGF-β1–induced EMT in lung fibrosis model via TGF-β signaling pathway.

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