倍他米松对大鼠雾化吸入镉诱导的炎症和肺气肿的影响。
Effects of betamethasone on inflammation and emphysema induced by cadmium nebulisation in rats.
作者信息
Fiévez Laurence, Kirschvink Nathalie, Zhang Wenhui H, Lagente Vincent, Lekeux Pierre, Bureau Fabrice, Gustin Pascal
机构信息
Department for Functional Sciences B41, Section of Pharmacology, Pharmacotherapy and Toxicology, Faculty of Veterinary Medicine, University of Liège, Liège, Belgium.
出版信息
Eur J Pharmacol. 2009 Mar 15;606(1-3):210-4. doi: 10.1016/j.ejphar.2009.01.020. Epub 2009 Jan 25.
Cadmium (Cd) induces centrilobular emphysema and is suspected to contribute to tobacco related lung diseases as chronic obstructive pulmonary disease (COPD). This study aimed to check whether the inflammatory process observed in rats exposed to nebulised Cd is resistant to betamethasone as observed in COPD and to determine the influence of this drug on airspace enlargement together with the MMP-2-9/TIMP-1-2 imbalance. Our results showed that betamethasone induced emphysema by itself in healthy rats. Moreover, pre-treatment of rats with betamethasone could only partially modulate the increase in bronchoalveolar lavage fluid cell counts and the absence of preventive effect of this compound against emphysema development is associated with its inability to rebalance the MMP-2-9/TIMP-1-2 ratio.
镉（Cd）可诱发小叶中心型肺气肿，并且被怀疑与诸如慢性阻塞性肺疾病（COPD）等烟草相关肺部疾病有关。本研究旨在检验雾化吸入镉的大鼠中观察到的炎症过程是否如在COPD中那样对倍他米松具有抗性，并确定该药物对气腔扩大以及MMP-2-9/TIMP-1-2失衡的影响。我们的结果表明，倍他米松自身可在健康大鼠中诱发肺气肿。此外，用倍他米松对大鼠进行预处理只能部分调节支气管肺泡灌洗液细胞计数的增加，并且该化合物对肺气肿发展缺乏预防作用与其无法使MMP-2-9/TIMP-1-2比值恢复平衡有关。
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