Early lung injury contributes to lung fibrosis via AT1 receptor in rats

doi:10.1111/j.1745-7254.2007.00493.x

CORC > 上海药物研究所 > 中国科学院上海药物研究所 > 药物安全性评价中心

	Early lung injury contributes to lung fibrosis via AT1 receptor in rats
	Chen, Fang-ping ; Gong, Li-kun; Zhang, Ling ; Wang, Hui ; Qi, Xin-ming; Wu, Xiong-fei ; Xiao, Ying ; Cai, Yan ; Liu, Lin-lin ; Li, Xiang-hong
刊名	ACTA PHARMACOLOGICA SINICA
	2007-02
卷号	28 期号:2 页码:227-237
关键词	angiotensin II AT1 receptor pulmonary fibrosis lung injury
ISSN号	1671-4083
DOI	10.1111/j.1745-7254.2007.00493.x
文献子类	Article
英文摘要	Aim: Angiotensin II is believed to play an important role in tissue repair and remodeling in lungs by the angiotensin type I (AT1) receptor via a number of potential mechanisms. However, the role of the AT1 receptor in early lung injury has not been characterized. Methods: Bleomycin-induced pulmonary fibrosis (PF) in rats was utilized to value the treatment with valsartan, an AT1 receptor antagonist, by measurement of body weight, wet weight of the left lung, hydroxyproline content, mRNA expression of collagen I/III, and the degree of fibrosis in lung tissues on d 21. Tissue injury in the early phase was assessed on d 1, 3 and 7 by apoptosis, malondialdehyde content, myeloperoxidase activity, inflammatory cell count and protein content. Angiotensin converting enzyme (ACE) activity and the AT1 receptor in lung tissues were analyzed by biochemistry method and Western blotting, respectively. Results: Valsartan ameliorated PF induced by bleomycin in the rats on d 21. After bleomycin was injected intratracheally, increases in the lung AT1 receptor and ACE activity were observed by d 1, 3 and 7. Lung injury deteriorated in the early phase. Valsartan reduced the increase of the AT1 receptor, ACE activity and lung injury induced by bleomycin in the early phase. Conclusion: These observations suggest that angiotensin II may play a potent role in early lung injury via the AT1 receptor. AT1 receptor antagonists should be assessed as potential new therapies for fibrotic lung disease.
WOS关键词	INDUCED PULMONARY-FIBROSIS ; ANGIOTENSIN-CONVERTING ENZYME ; TYPE-1 RECEPTOR ; ENDOTHELIAL-CELLS ; INDUCED APOPTOSIS ; OXIDATIVE STRESS ; EPITHELIAL-CELLS ; DE-NOVO ; CAPTOPRIL ; DISEASE
WOS研究方向	Chemistry ; Pharmacology & Pharmacy
语种	英语
CSCD记录号	CSCD:2845196
出版者	BLACKWELL PUBLISHING
WOS记录号	WOS:000243697900011
内容类型	期刊论文
源URL	[http://119.78.100.183/handle/2S10ELR8/273330]
专题	药物安全性评价中心中科院受体结构与功能重点实验室新药研究国家重点实验室
通讯作者	Ren, Jin
作者单位	1.Chinese Acad Sci, Shanghai Inst Biol Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Shanghai 201203, Peoples R China 2.Shanghai Pulm Hosp, Shanghai 200043, Peoples R China 3.Chinese Acad Sci, Grad Sch, Shanghai Branch, Shanghai 200031, Peoples R China
推荐引用方式 GB/T 7714	Chen, Fang-ping,Gong, Li-kun,Zhang, Ling,et al. Early lung injury contributes to lung fibrosis via AT1 receptor in rats[J]. ACTA PHARMACOLOGICA SINICA,2007,28(2):227-237.
APA	Chen, Fang-ping.,Gong, Li-kun.,Zhang, Ling.,Wang, Hui.,Qi, Xin-ming.,...&Ren, Jin.(2007).Early lung injury contributes to lung fibrosis via AT1 receptor in rats.ACTA PHARMACOLOGICA SINICA,28(2),227-237.
MLA	Chen, Fang-ping,et al."Early lung injury contributes to lung fibrosis via AT1 receptor in rats".ACTA PHARMACOLOGICA SINICA 28.2(2007):227-237.