Intermittent hypoxia with or without hypercapnia is associated with tumorigenesis by decreasing the expression of brain derived neurotrophic factor and miR-34a in rats

Zhang Jing; Guo Xu; Shi Yanwei; Ma Jing; Wang Guangfa

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Intermittent hypoxia with or without hypercapnia is associated with tumorigenesis by decreasing the expression of brain derived neurotrophic factor and miR-34a in rats

机译：伴或不伴高碳酸血症的间歇性缺氧与肿瘤发生有关，可通过降低大鼠脑源性神经营养因子和miR-34a的表达来实现

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Background Very recent studies revealed that obstructive sleep apnoea (OSA) is a contributor of the increased incidence and mortality of cancer in humans,but mechanisms of how OSA promotes tumorigenesis remains largely unknown.We investigated whether intermittent hypoxia with and without hypercapnia plays a role in tumorigenesis.Methods First,Sprague-Dawley (SD) male rats (12 weeks old) were subjected to different hypoxia exposures:intermittent hypoxia and intermittent hypoxia with hypercapnia; continuous hypoxia and normal air.The systemic application of chronic fast rate hypoxia with or without hypercapnia mimicked severe OSA patients with apnoea/hypopnea index equivalent to 60 events per hour.Then routine blood tests were performed and the levels of brain derived neurotrophic factor (BDNF) and miR-34a were examined.Results In contrast to intermittent hypoxia with hypercapnia,both intermittent hypoxia and continuous hypoxia treatments caused significantly higher levels of haematology parameters than normoxia treatments.Compared to normoxia,intermittent hypoxia with hypercapnia exposure resulted in substantial decrease of serum BDNF and,miR-34a in the lower brainstem,while less pronounced results were found in intermittent hypoxia and continuous hypoxia exposure.Conclusions The exposure of intermittent hypoxia with or without hypercapnia,mimicking the situations in severe OSA patients,was associated with,or even promoted tumorigenesis.

机译：背景技术最近的研究表明阻塞性睡眠呼吸暂停（OSA）是人类癌症发病率和死亡率增加的原因，但是OSA促进肿瘤发生的机制尚不清楚。我们调查了间歇性缺氧在有无高碳酸血症的情况下是否起作用。方法首先，对12周大的Sprague-Dawley（SD）雄性大鼠进行不同的缺氧暴露：间歇性缺氧和间歇性缺氧合并高碳酸血症;持续性缺氧和正常空气。全身快速慢性缺氧有或没有高碳酸血症的应用模拟了重度OSA呼吸暂停/呼吸不足指数等于每小时60事件的OSA患者，然后进行常规血液检查和脑源性神经营养因子（BDNF）水平结果与间歇性缺氧合并高碳酸血症相比，间歇性缺氧和连续性缺氧治疗均导致血液学参数水平明显高于正常氧治疗。与正常氧相比，间歇性缺氧合并高碳酸血症导致血清显着减少。 BDNF和miR-34a位于下脑干中，而间歇性缺氧和持续性缺氧暴露的结果较不明显。结论间歇性缺氧伴或不伴高碳酸血症的暴露，与严重OSA患者的情况相似，甚至与甚至促进肿瘤发生。

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《中华医学杂志（英文版）》 |2014年第1期|43-47|共5页
作者
Zhang Jing; Guo Xu; Shi Yanwei; Ma Jing; Wang Guangfa;
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Department of Respiratory and Critical Care Medicine, Peking University First Hospital, Beijing 100034, China;

Department of Neurosurgery, Liaoning Cancer Hospital & Institute, Shenyang, Liaoning 110042, China;

Department of Respiratory Medicine, Peking University Shougang Hospital, Beijing 100041, China;

Department of Respiratory and Critical Care Medicine, Peking University First Hospital, Beijing 100034, China;

Department of Respiratory and Critical Care Medicine, Peking University First Hospital, Beijing 100034, China;

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收录信息中国科学引文数据库(CSCD);中国科技论文与引文数据库(CSTPCD);
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Intermittent hypoxia with or without hypercapnia is associated with tumorigenesis by decreasing the expression of brain derived neurotrophic factor and miR-34a in rats

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