| Neuropeptide substance P attenuates hyperoxia-induced oxidative stress injury in type II alveolar epithelial cells via suppressing the activation of JNK pathway. | |
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MedLine Citation:
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PMID: 19789913 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Hyperoxia-induced oxidative stress plays a key role in many pulmonary diseases. In an earlier study we found the protective effect of the neuropeptide substance P (SP) on type II alveolar epithelial cells (AECIIs) after hyperoxia exposure. Then, we investigated c-Jun N-terminal kinase (C-JNK) signal transduction pathways in AECIIs before and after hyperoxia exposure. Primary AECIIs were isolated and purified from premature rats. Subsequently, the cells were treated with air (21% oxygen), hyperoxia (95% oxygen), SP+ air, and SP+ hyperoxia. SP was added in advance to reach a final concentration 1 x 10(-6) mol/l. The cells were then exposed to air and hyperoxia for 12, 24, and 48 h. XTT cell proliferation assay and fluorescence-activated cell sorting (FACS) were employed to detect cell growth and apoptosis. Phosphorylated JNK (p-JNK) levels were measured using Western blot assay. The morphological alteration of AECIIs was observed using a transmission electron microscope (TEM). Compared with the simple hyperoxia treatment, the cell growth and apoptosis percentage was significantly increased and decreased after adding additional SP. Meanwhile, the reduced levels of p-JNKs could be found after adding SP. Furthermore, the morphological damage of AECIIs was greatly improved. These data suggest that SP can promote AECII proliferation and inhibit apoptosis by suppressing JNK signal pathways after hyperoxia exposure, which attenuates hyperoxia-induced oxidative stress damage in AECIIs. It might be a potential therapy for acute pulmonary injury under hyperoxia-induced oxidative stress. |
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Authors:
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Bo Huang; Hongmin Fu; Ming Yang; Fang Fang; Fengwu Kuang; Feng Xu |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-09-30 |
Journal Detail:
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Title: Lung Volume: 187 ISSN: 1432-1750 ISO Abbreviation: Lung Publication Date: 2009 Nov-Dec |
Date Detail:
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Created Date: 2010-01-21 Completed Date: 2010-03-24 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7701875 Medline TA: Lung Country: United States |
Other Details:
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Languages: eng Pagination: 421-6 Citation Subset: IM |
Affiliation:
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Children's Hospital of Chongqing Medical University, 136 Zhongshan No. 2 Road, Yu Zhong District, Chongqing, 400014, China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acute Lung Injury
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etiology,
prevention & control* Animals Apoptosis / drug effects Cell Proliferation Cytoprotection* Hyperoxia / complications* JNK Mitogen-Activated Protein Kinases / antagonists & inhibitors* Oxidative Stress / drug effects Pulmonary Alveoli / drug effects*, enzymology, ultrastructure Rats Rats, Sprague-Dawley Respiratory Mucosa / drug effects, enzymology, ultrastructure Substance P / pharmacology*, physiology |
| Chemical | |
Reg. No./Substance:
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33507-63-0/Substance P; EC 2.7.11.24/JNK Mitogen-Activated Protein Kinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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