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Apoptosis and Inflammation Associated Gene Expressions in Monocrotaline-Induced Pulmonary Hypertensive Rats after Bosentan Treatment

Title
Apoptosis and Inflammation Associated Gene Expressions in Monocrotaline-Induced Pulmonary Hypertensive Rats after Bosentan Treatment
Authors
Hong, Young MiKwon, Jung HyunChoi, ShinkyuKim, Kwan Chang
Ewha Authors
홍영미김관창최신규권정현
SCOPUS Author ID
홍영미scopus; 김관창scopus; 최신규scopus
Issue Date
2014
Journal Title
KOREAN CIRCULATION JOURNAL
ISSN
1738-5520JCR Link1738-5555JCR Link
Citation
vol. 44, no. 2, pp. 97 - 104
Keywords
Hypertension, pulmonaryMonocrotalineApoptosisGene expressionBosentan
Publisher
KOREAN SOC CARDIOLOGY
Indexed
SCIE; SCOPUS; KCI WOS scopus
Abstract
Background and Objectives: Vascular wall remodeling in pulmonary hypertension can be caused by an aberration in the normal balance between proliferation and apoptosis of endothelial cell in the pulmonary artery. The objective of this study was to evaluate the effect of bosentan on apoptosis in monocrotaline (MCT)-induced pulmonary hypertension. Materials and Methods: Sprague-Dawley rats were divided into three groups: control (C) group, M group (MCT 60 mg/kg) and B group (MCT 60 mg/kg plus bosentan 20 mg/day orally). Gene expressions of Bcl (B cell leukemia/lymphoma)-2, caspase-3, complement component (C)-6, vascular endothelial growth factor (VEGF), interleukin (IL)-6 and tumor necrosis factor-alpha (TNF-alpha) were analyzed by real time polymerase chain reaction and western blot analysis. Results: The messenger ribonucleic acid (mRNA) expressions of caspase-3 and VEGF were significantly increased in the M group compared with the C group, and significantly decreased in the B group compared with the M group in week 4. mRNA expression of IL-6 was significantly decreased in weeks 1, 2, and 4 in the B group compared with the M group. mRNA expression of TNF-alpha was significantly decreased on day 5 and in weeks 1 and 2 in the B group compared with the M group. Conclusion: Bosentan may have potential for preventing apoptosis and inflammation.
DOI
10.4070/kcj.2014.44.2.97
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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