HJP272, A Novel Endothelin Receptor Antagonist, Attenuates Lipopolysaccharide-Induced Acute Lung Injury in Hamsters
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- 作者：Shikha Patel (1)
Xingjian Liu (1)
Ming Liu (2)
Ralph Stephani (1)
Hardik Patel (1)
Jerome Cantor (1) - 关键词：Endothelin ; Lipopolysaccharide ; Endothelin receptor antagonist ; Neutrophils ; Acute lung injury
- 刊名：Lung
- 出版年：2014
- 出版时间：October 2014
- 年：2014
- 卷：192
- 期：5
- 页码：803-810
- 全文大小：609 KB
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Xingjian Liu (1)
Ming Liu (2)
Ralph Stephani (1)
Hardik Patel (1)
Jerome Cantor (1)
1. College of Pharmacy and Health Sciences, St John鈥檚 University, Queens, NY, USA
2. Department of Pathology, Brookdale Hospital and Medical Center, Brooklyn, NY, USA - ISSN：1432-1750
文摘
Introduction Previous studies from this laboratory indicate that endothelin-1 (ET-1), a potent vasoconstrictor, may play an important role in lipopolysaccharide (LPS)-induced release of neutrophils from the pulmonary microvasculature. To further test this concept, Syrian hamsters were treated with a novel endothelin receptor A (ETA) antagonist (HJP272) prior to intratracheal instillation of LPS. Methods The effect of HJP272 on the LPS-induced inflammatory reaction was determined by measuring: (1) lung histopathological changes, (2) total neutrophils in bronchoalveolar lavage fluid (BALF), (3) expression of tumor necrosis factor receptor 1 (TNFR1) by BALF macrophages, and (4) alveolar septal cell apoptosis. Results Treatment with HJP272 significantly reduced each of these parameters during a 24-hr period following LPS instillation, supporting the concept that limiting the activity of ET-1 may reduce the extent of lung injury. This hypothesis was further tested by giving ET-1 prior to LPS instillation, which resulted in a marked enhancement of LPS-induced lung inflammation, as measured by BALF neutrophils and TNFR1-positive macrophages. Furthermore, the increase in neutrophils resulting from treatment with ET-1 was significantly reduced by HJP272, again demonstrating the ability of ETA receptor antagonists to limit the influx of these cells into the lung. Conclusions These findings suggest a potential therapeutic role for these agents in diseases where neutrophils are a significant cause of lung injury, such as bronchopneumonia, respiratory distress syndrome, and chronic obstructive pulmonary disease.