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首页> 外文期刊>American Journal of Physiology >COX-2-derived prostacyclin protects against bleomycin-induced pulmonary fibrosis.
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COX-2-derived prostacyclin protects against bleomycin-induced pulmonary fibrosis.

机译：源自COX-2的前列环素可预防博来霉素诱导的肺纤维化。

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摘要

Prostacyclin is one of a number of lipid mediators elaborated from the metabolism of arachidonic acid by the cyclooxygenase (COX) enzymes. This prostanoid is a potent inhibitor of platelet aggregation, and its production by endothelial cells and protective role in the vasculature are well established. In contrast, much less is known regarding the function of this prostanoid in other disease processes. We show here that COX-2-dependent production of prostacyclin plays an important role in the development of fibrotic lung disease, limiting both the development of fibrosis and the consequential alterations in lung mechanics. In stark contrast, loss of prostaglandin E(2) synthesis and signaling through the G(s)-coupled EP2 and EP4 receptors had no effect on the development of disease. These findings suggest that prostacyclin analogs will protect against bleomycin-induced pulmonary fibrosis in COX-2(-/-) mice. If such protection is observed, investigation of these agents as a novel therapeutic approach to pulmonary fibrosis in humans may be warranted.
机译：前列环素是通过环氧合酶（COX）酶从花生四烯酸的代谢中阐明的许多脂质介体之一。该类前列腺素是血小板聚集的有效抑制剂，并且已经很好地确定了其由内皮细胞产生和在脉管系统中的保护作用。相反，关于这种前列腺素在其他疾病过程中的功能的了解还很少。我们在这里显示，依赖COX-2的前列环素的产生在纤维化性肺病的发展中起着重要作用，既限制了纤维化的发展，也限制了肺力学的相应改变。与之形成鲜明对比的是，前列腺素E（2）的合成和信号通过G（s）耦合的EP2和EP4受体的丢失对疾病的发展没有影响。这些发现表明前列环素类似物将防止博莱霉素诱导的COX-2（-/-）小鼠肺纤维化。如果观察到这种保护，则可能需要对这些药物进行研究，以作为治疗人类肺纤维化的一种新颖方法。

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