慢性间歇性缺氧对大鼠肺组织凋亡相关基因Bcl-2、Bax表达的影响

目的探讨凋亡(apoptosis)相关基因Bcl-2、Bax在慢性间歇性缺氧(chronic intermittent hypoxia,CIH)大鼠肺组织中的表达,明确其与阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hypopnea syndrome,OSAHS)肺部病变的关系.方法取健康雄性Sprague-Dawley(S-D)大鼠20只,随机分为正常对照组(A组)和CIH组(B组),每组10只,根据实验要求,将B组大鼠暴露于CIH的环境中,8h/d(上午9时至下午5时),共5w,以模拟OSAHS患者CIH的特征.A组大鼠常规饲养,不予以任何处理.采用免疫组织化学方法(SP法)检测大鼠肺组织中Bcl-2、Bax蛋白的表达.结果大鼠肺组织中阳性细胞表达部位主要集中于支气管上皮细胞和肺泡上皮细胞.正常大鼠Bcl-2、Bax蛋白均有基础低表达,经CIH处理后可见大鼠支气管上皮细胞和肺泡上皮细胞Bcl-2、Bax蛋白表达的上调和Bax/bcl-2比值的升高.结论 CIH可导致大鼠肺组织细胞凋亡的增加,凋亡参与了CIH大鼠肺部病变的病理生理过程;Bcl-2和Bax这一对凋亡抑制和促进基因参与了CIH过程中大鼠肺组织细胞凋亡的调控.

EXPRESSION OF APOPTOSIS-RELATED GENES BCL-2 AND BAX IN LUNG TISSUES OF RATS WITH CHRONIC INTERMITTENT HYPOXIA

Objective To investigatethe expression of some apoptosis-related genes(Bcl-2andBax) in lung tissues of rats with chronic intermittent hypoxia(CIH)and their relationship to the pathogenesis of obstructive sleep apnea hypopnea syndrome(OSAHS).Methods 20 healthy male SD rats were randomly assigned to two equal groups: the control group(group A)and the CIH group(group B).The rats in group B were exposed to alternating periods of hypoxia and normoxia once per minute for 8h/d(from 9AM to 5PM) for 5 weeks in order to mimic the intermittent hypoxia of OSAHS in humans,while the rats in group A were raised without any treatment.The expression of Bcl-2 and Bax proteins in lung tissues ofthe rats wereexamined immunohistochemically.Results The expression of Bcl-2 and Bax proteins was up-regulated significantly in lung tissues(bronchus and alveolar epithelial cells) of rats with CIH compared with those of the control group;furthermore,the rate of Bax/Bcl-2 increased significantly in the CIH group.Conclusion CIH can increase apoptosisin lung tissuesof rats andapoptosis has participated in the disorderof lungtissuesof rats with CIH;apoptosis-relatedgenes(Bcl-2and Bax) takepart in the regulation of apoptosis in lung tissuesof ratswith CIH.