Cigarette smoke-mediated oxidative stress induces apoptosis via the MAPKs/STAT1 pathway in mouse lung fibroblasts
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- 作者：Hanbyeol Leea ; Jeong-Ran Parka ; Eun-Jeong Kima ; Woo Jin Kimb ; Seok-Ho Hongb ; Sung-Min Parka ; Se-Ran Yanga ; seran@knagwon.ac.kr" class="auth_mail" title="E-mail the corresponding author ; seran.yang@gmail.com" class="auth_mail" title="E-mail the corresponding author
- 关键词：COPD ; chronic obstructive pulmonary disease ; CS ; cigarette smoke ; CSE ; cigarette smoke extracts ; ROS ; reactive oxygen species ; NO ; nitric oxide ; SOD ; superoxide dismutase ; GSH ; glutathione ; DCF-DA ; 2&prime ; 7&prime ; - dichlorofluorescin diacetate ; Bax ; Bcl2-associated X protein ; Bcl-2 ; B-cell CLL/lymphoma 2 ; COX- 2 ; cyclooxygenase-2 ; TNF-α ; tumor necrosis factor alpha ; IL-6 ; interleukin-6 ; MAPK ; mitogen-activated protein kinase ; STAT1 ; signal transducer and activator of transcription1
- 刊名：Toxicology Letters
- 出版年：2016
- 出版时间：5 January 2016
- 年：2016
- 卷：240
- 期：1
- 页码：140-148
- 全文大小：1760 K
文摘
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CSE decreased the proliferation of mouse lung fibroblasts, which is essential for the maintenance of extracellular matrix.
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CSE caused an abnormal inflammatory response and ROS/RNS-mediated stress by an imbalance in the cellular antioxidant defense system (GSH recycling and SOD activity), leading to the apoptosis of lung parenchymal fibroblasts.
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The apoptosis of lung fibroblasts, through the phosphorylation of STAT1 at Tyr701/Ser727 and the up-regulation of the MAPK pathway by CSE, contributes to the pathogenesis of COPD.