Immunohistochemical detection of apoptotic proteins, p53/Bax and JNK/FasL cascade, in the lung of rats exposed to cigarette smoke.

doi:10.1007/s00204-005-0050-4

中山醫學大學機構典藏 CSMUIR > 醫學院 > 生化微生物免疫研究所 > 期刊論文 > Item 310902500/10788

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/10788

Title:	Immunohistochemical detection of apoptotic proteins, p53/Bax and JNK/FasL cascade, in the lung of rats exposed to cigarette smoke.
Authors:	Wu, CH Lin, HH Yan, FP Wu, CH Wang, CJ
Contributors:	中山醫學大學
Keywords:	Cigarette smoke;Lung pathogenesis;Cleaved caspase-3;Bax;Phospho-p53;Phospho-JNK;FasL
Date:	2006
Issue Date:	2015-05-11T09:51:05Z (UTC)
ISSN:	0340-5761
Abstract:	Lung disease is the leading and second-leading cause of death in women and men in Taiwan, respectively. Epidemiological studies conducted in Taiwan have shown that cigarette smoking is the principal risk factor of lung disease, but little is known about the association between apoptosis and cigarette smoke (CS)-induced lung pathogenesis. We designed an animal exposure system to study signal proteins involved in the process of apoptosis induced by smoking in rat terminal bronchiole. Rats were exposed to CS in doses of 5, 10, and 15 cigarettes, respectively, and the exposure lasted for 30 min, twice a day, 6 days a week for 1 month. Following which the rats were sacrificed and the lung tissues were analyzed by histopathological methods. The terminal bronchioles revealed mild to severe inflammation according to the doses of CS and marked lipid peroxidation, lymphocyte infiltration, congestion, and epithelial emphysema of alveolar spaces were also noted. Using an in situ cell death detection kit (TA300), the association of CS with apoptosis was determined in a concentration-dependent manner. Immunohistochemical evaluation showed that CS treatment produced an increase in the cellular levels of Bax, t-Bid, cleaved caspase-3, phospho-p53, phospho-JNK, and FasL but a decline in Bcl-2 and Mcl-1 (p<0.001 for all) in rat terminal bronchioles. The results provided evidences suggesting that exposure to CS not only induced apoptosis, but also involved p53/Bax and JNK/FasL cascade pathway.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/10788 http://dx.doi.org/10.1007/s00204-005-0050-4
Relation:	Arch Toxicol. 2006 Jun;80(6):328-36. Epub 2005 Dec 9.
Appears in Collections:	[生化微生物免疫研究所] 期刊論文

Files in This Item:

File	Description	Size	Format
index.html	期刊論文	0Kb	HTML	287	View/Open

View Licence

Loading...