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http://dx.doi.org/10.4070/kcj.2014.44.2.97

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

Hong, Young Mi (Department of Pediatrics, Ewha Womans University School of Medicine)
Kwon, Jung Hyun (Department of Pediatrics, Ewha Womans University School of Medicine)
Choi, Shinkyu (Department of Physiology, Ewha Womans University School of Medicine)
Kim, Kwan Chang (Department of Thoracic & Cardiovascular Surgery, Ewha Womans University School of Medicine)
Publication Information
Korean Circulation Journal / v.44, no.2, 2014 , pp. 97-104 More about this Journal
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.
Keywords
Hypertension, pulmonary; Monocrotaline; Apoptosis; Gene expression; Bosentan;
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