Next Article in Journal
Bioresorbable Drug-Eluting Magnesium-Alloy Scaffold for Treatment of Coronary Artery Disease
Previous Article in Journal
Oxidative Stress and Neurodegenerative Disorders
Open AccessArticle

Atorvastatin Attenuates Bleomycin-Induced Pulmonary Fibrosis via Suppressing iNOS Expression and the CTGF (CCN2)/ERK Signaling Pathway

by 1, 2,*, 1 and 1
1
Department of Pulmonary and Critical Care Medicine, the First Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710061, China
2
Department of Cardiology, the First Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710061, China
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2013, 14(12), 24476-24491; https://doi.org/10.3390/ijms141224476
Received: 14 October 2013 / Revised: 28 November 2013 / Accepted: 3 December 2013 / Published: 16 December 2013
(This article belongs to the Section Biochemistry)
Pulmonary fibrosis is a progressive and fatal lung disorder with high mortality rate. To date, despite the fact that extensive research trials are ongoing, pulmonary fibrosis continues to have a poor response to available medical therapy. Statins, 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, known for its broad pharmacological activities, remains a remedy against multiple diseases. The present study investigated the antifibrotic potential of atorvastatin against bleomycin-induced lung fibrosis and to further explore the possible underlying mechanisms. Our results showed that atorvastatin administration significantly ameliorated the bleomycin mediated histological alterations and blocked collagen deposition with parallel reduction in the hydroxyproline level. Atorvastatin reduced malondialdehyde (MDA) level and lung indices. Atorvastatin also markedly decreased the expression of inducible nitric oxide synthase (iNOS) in lung tissues and, thus, prevented nitric oxide (NO) release in response to bleomycin challenge. Furthermore, atorvastatin exhibited target down-regulation of connective tissue growth factor (CTGF (CCN2)) and phosphorylation extracellular regulated protein kinases (p-ERK) expression. Taken together, atorvastatin significantly ameliorated bleomycin-induced pulmonary fibrosis in rats, via the inhibition of iNOS expression and the CTGF (CCN2)/ERK signaling pathway. The present study provides evidence that atorvastatin may be a potential therapeutic reagent for the treatment of lung fibrosis. View Full-Text
Keywords: pulmonary fibrosis; atorvastatin; iNOS; CTGF (CCN2); ERK pulmonary fibrosis; atorvastatin; iNOS; CTGF (CCN2); ERK
MDPI and ACS Style

Zhu, B.; Ma, A.-Q.; Yang, L.; Dang, X.-M. Atorvastatin Attenuates Bleomycin-Induced Pulmonary Fibrosis via Suppressing iNOS Expression and the CTGF (CCN2)/ERK Signaling Pathway. Int. J. Mol. Sci. 2013, 14, 24476-24491.

Show more citation formats Show less citations formats

Article Access Map by Country/Region

1
Only visits after 24 November 2015 are recorded.
Search more from Scilit
 
Search
Back to TopTop