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用诺龙治疗后肺气肿仓鼠膈肌的线粒体功能

Mitochondrial function in diaphragm of emphysematous hamsters after treatment with nandrolone.

作者信息

Wijnhoven Hanneke J H, Ennen Leo, Rodenburg Richard J T, Dekhuijzen P N Richard

机构信息

Department of Pulmonary Diseases, Institute for Fundamental and Clinical Human Movement Sciences, Radboud University, Nijmegen Medical Centre, Nijmegen, The Netherlands.

出版信息

Int J Chron Obstruct Pulmon Dis. 2006;1(1):83-9. doi: 10.2147/copd.2006.1.1.83.

DOI:10.2147/copd.2006.1.1.83
PMID:18046906
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2706598/
Abstract

Respiratory failure in patients with COPD may be caused by insufficient force production or insufficient endurance capacity of the respiratory muscles. Anabolic steroids may improve respiratory muscle function in COPD. The effect of anabolic steroids on mitochondrial function in the diaphragm in emphysema is unknown. In an emphysematous male hamster model, we investigated whether administration of the anabolic steroid nandrolone decanoate (ND) altered the activity of mitochondrial respiratory chain complexes in the diaphragm. The bodyweight of hamsters treated with ND was decreased after treatment compared with initial values, and serum testosterone levels were significantly lower in hamsters treated with ND than in control hamsters. No difference in the activity of mitochondrial respiratory chain complexes in the diaphragm between normal and emphysematous hamsters was observed. Treatment with ND did not change the activity of mitochondrial respiratory chain complexes in the diaphragm of both normal and emphysematous hamsters. In emphysematous hamsters, administration of ND decreased the activity of succinate:cytochrome c oxidoreductase compared with ND treatment in normal hamsters. We conclude that anabolic steroids have negative effects on the activity of succinate:cytochrome c oxidoreductase and anabolic status in this emphysematous hamster model.

摘要

慢性阻塞性肺疾病(COPD)患者的呼吸衰竭可能是由呼吸肌力量产生不足或耐力不足所致。合成代谢类固醇可能改善COPD患者的呼吸肌功能。合成代谢类固醇对肺气肿患者膈肌线粒体功能的影响尚不清楚。在一个肺气肿雄性仓鼠模型中,我们研究了给予合成代谢类固醇癸酸诺龙(ND)是否会改变膈肌线粒体呼吸链复合物的活性。与初始值相比,接受ND治疗的仓鼠体重在治疗后下降,且接受ND治疗的仓鼠血清睾酮水平显著低于对照仓鼠。在正常仓鼠和肺气肿仓鼠的膈肌中,未观察到线粒体呼吸链复合物活性的差异。ND治疗并未改变正常仓鼠和肺气肿仓鼠膈肌中线粒体呼吸链复合物的活性。在肺气肿仓鼠中,与正常仓鼠接受ND治疗相比,给予ND降低了琥珀酸:细胞色素c氧化还原酶的活性。我们得出结论,在这个肺气肿仓鼠模型中,合成代谢类固醇对琥珀酸:细胞色素c氧化还原酶的活性和合成代谢状态有负面影响。

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