慢性间歇低氧对大鼠肺组织损伤及依达拉奉的干预作用

寇育乐; 解宝泉; 王红阳; 张嘉宾; 谭曦舒; 张敏

doi:10.13201/j.issn.1001-1781.2015.19.014

慢性间歇低氧对大鼠肺组织损伤及依达拉奉的干预作用

- 华北理工大学附属医院呼吸科(河北唐山, 063000)
基金项目:
河北省重大医学科研课题(No:zd2013091)

详细信息

通讯作者: 王红阳,E-mail:tsmywhy@163.com

中图分类号: R563.8

收稿日期: 2015-07-22

The pulmonary injury in rats caused by chronic intermittent hypoxia and the intervention effect of Edaravone

- Department of Respiration of North China University of Science and Technology Hospital, Tangshan, 063000, China

More Information

Corresponding author: WANG Hongyang, E-mail: tsmywhy@163.com

Received Date: 22 July 2015

摘要

摘要: 目的: 探讨慢性间歇低氧(CIH)对大鼠肺损伤的机制和依达拉奉的干预作用及可能机制。方法: 采用随机数字表法将96只雄性Wistar大鼠随机分为正常对照组(UC组)、间歇低氧组(CIH组)、依达拉奉治疗组(NE组)、低氧生理盐水组(NS组),各亚组持续时间分别为1、2、3、4周,每个亚组6只大鼠。实验结束后分别观察各亚组大鼠肺组织苏木精-伊红病理变化、血气检测血氧分压(PO₂),采用化学法检测肺组织MDA含量和SOD活性,实时荧光定量PCR检测Ang Ⅱ mRNA。结果: UC组未见明显病理损害,而CIH组肺泡壁水肿增厚,肺泡融合,肺间质及支气管上皮内也可见中性粒细胞浸润,且随时间延长,病理损伤逐渐加重;与NS组相比,NE组出现病理损伤的时间较晚且程度较轻;各组亚组内PO₂未见差异;与UC组同一时间点比较,CIH组PO₂明显降低,而NE组较NS组有所恢复;与UC及NE组比较,CIH组及NS组MDA含量于各个时间点均逐渐增加(P<0.05),SOD活性于各个时间点均逐渐减少(P<0.05);Ang Ⅱ mRNA的表达于各个时间点增加,于4周达高峰;与CIH组比较,NE组各指标的变化过程受到抑制(P<0.05)。CIH组Ang Ⅱ mRNA与SOD呈负相关(r=-0.904,P<0.01);Ang Ⅱ mRNA与MDA呈正相关(r=0.782,P<0.01)。结论: 慢性间歇低氧可通过氧化应激和激活 AngⅡ导致肺组织损伤,依达拉奉可能通过清除氧自由基,从而抵抗间歇低氧所致肺损伤。
- 睡眠呼吸暂停低通气综合征 /
- 阻塞性 /
- 间歇性低氧 /
- 氧化应激 /
- 血管紧张素Ⅱ /
- 依达拉奉
Abstract: Objective: To investigate the mechanism of the pulmonary injury in rats caused by chronic intermittent hypoxia(CIH) and to investigate the intervention effect of Edaravone.Method: Ninety-six male Wistar rats were divided into four groups randomly:the control group (NC), chronic intermittent hypoxia group (CIH), chronic intermittent hypoxia normal saline matched group(NS), chronic intermittent hypoxia edaravone treatment group (NE). The four groups were also divided into 1, 2, 3, 4 W time subgroups, and each time subgroup had 6 rats. After the experiment, sections of pulmonary were stained with hematoxylin-eosin (HE) and the level of SOD,MDA,PO₂ and AngⅡmRNA in rat homogenate pulmonary were measured.Result: Pulmonary histology revealed that the CIH group showed high levels of interstitial edema, alveolar atelectasis, inflammatory cell infiltration of alveolar epithelial cell, pulmonary injury were serious in 1,2,3,4 W. But the pulmonary histology of the UC group and the NS group was normal. Compared with the NS group, pulmonary injury of NE group 1, 2,3,4 W, significantly decreased. Compared with the NC group,the levels of PO₂ in the CIH group were decreased; while the compared with the NS group, the levels of PO₂ in the NE group were increased. Compared with the UC group and NS group, the levels of AngⅡmRNA in each time point in CIH group were increased gradually (P<0.05), the content of MDA were increased in 1, 2, 3, 4 W (P<0.05), they had reached the peak all at 4 W; while the SOD in each time point in CIH group were decreased gradually (P<0.05) compared with that in UC group and NS group; The AngⅡmRNA levels of CIH in pulmonary showed positive correlation with MDA[r=0.782,P<0.01];while the AngⅡmRNA levels of CIH in pulmonary showed negative correlation with SOD[r=-0.904, P<0.01].Conclusion: CIH can cause pulmonary injury through oxidative stress and activating AngⅡ, and Edaravone could prevent pulmonary injury induced by CIH through scavenging oxygen free radicals.
- sleep apnea hypopnea syndrome obstructive /
- chronic intermittent hypoxia /
- oxidation stress /
- an-giotensin Ⅱ /
- Edaravone /

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