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急性减压缺氧对大鼠肺组织损伤的研究
  • ISSN号:2095-140X
  • 期刊名称:《解放军医药杂志》
  • 时间:0
  • 分类:R594.3[医药卫生—临床医学;医药卫生—内科学] R-332[医药卫生]
  • 作者机构:[1]兰州大学药学院,兰州730000, [2]兰州军区兰州总医院全军高原环境损伤防治重点实验室,兰州730050
  • 相关基金:国家自然科学基金项目(81571847); 甘肃省自然科学基金(145RJZA089); 全军医药卫生科研基金(CLZ14JA01,LZ13GY07)
中文摘要:

目的观察氧化应激相关指标在模拟急进高原缺氧大鼠肺组织的变化情况。方法成年健康雄性Wistar大鼠40只,随机分为正常对照组、缺氧1、3、5 d组,每组10只。观察缺氧不同时间大鼠肺组织病理学的改变情况,检测肺组织相关生化指标水平。结果缺氧各组大鼠肺组织均有明显损伤,且以缺氧3 d组大鼠损伤尤为严重。与正常对照组比较,缺氧各组大鼠肺组织总抗氧化能力(total antioxidant capacity,TAOC)、还原型谷胱甘肽(reduced glutathione,GSH)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-PX)、总一氧化氮合酶(total nitric oxide synthase,TNOS)和乳酸脱氢酶(lactate dehydrogenase,LDH)在缺氧3 d组显著降低(P〈0.05,P〈0.01),丙二醛(maleic dialdehyde,MDA)、乳酸(lactate,LD)含量显著升高(P〈0.01),且随缺氧时间的延长逐渐增加;总超氧化物歧化酶(total superoxide dismutase,TSOD)、Na^+K^+-ATP酶活力显著降低(P〈0.05,P〈0.01),一氧化氮(nitric oxide,NO)含量在缺氧1、3 d组明显降低(P〈0.01)。结论急进高原缺氧大鼠肺损伤机制与氧化应激反应有关,机体抗氧化能力降低、自由基增加是导致肺组织损伤的重要因素,且损伤程度与缺氧暴露时间有关。

英文摘要:

Objective To observe changes of related indexes of oxidative stress in lung tissues of rats under simula-ted acute depression and hypoxia environment. Methods A total of 40 adult male Wistar rats were randomly divided into con-trol group and 1, 3 and 5 d hypoxia groups (n=10 for each group). Pathological changes of lung tissues at different exposure times were observed, and related indexes of lung tissues were detected in rats. Results Lung tissues of all hypoxia groups were obviously damaged, and the significant damage was found in 3 d hypoxia group. Compared with those in control group, in hypoxia groups, levels of total antioxidant capacity ( TAOC) , reduced glutathione ( GSH) , glutathione peroxidase ( GSH-PX) , total nitric oxide synthase (TNOS) and lactate dehydrogenase (LDH) were decreased, and the most decreased levels were found in 3 d hypoxia group (P〈0. 05, P〈0. 01);contents of maleic dialdehyde (MDA) and lactic acid (LD) were signifi-cantly increased (P〈0. 01), and the contents were gradually increased with prolonged hypoxia time;activities of total super-oxide dismutase (TSOD) and Na+K+-ATP enzyme were significantly decreased (P〈0. 05, P〈0. 01);contents of nitric oxide (NO) were significantly decreased in 1 and 3 d hypoxia groups (P〈0. 01). Conclusion Mechanisms of damage in lung tis-sues of rats relate to oxidative stress reaction under simulated acute depression and hypoxia environment. The decreasing an-tioxidant capacity of the body and increasing free radicals are the important factors leading to damage of lung tissues, and de-gree of lung damage relates to exposure time in depression and hypoxia environment.

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期刊信息
  • 《解放军医药杂志》
  • 中国科技核心期刊
  • 主管单位:北京军区联勤部卫生部
  • 主办单位:北京军区医学科学技术委员会
  • 主编:赵会懂
  • 地址:石家庄市中山西路398号
  • 邮编:050082
  • 邮箱:jfjyyzz@126.com
  • 电话:0311-87978599
  • 国际标准刊号:ISSN:2095-140X
  • 国内统一刊号:ISSN:13-1406/R
  • 邮发代号:18-232
  • 获奖情况:
  • 国内外数据库收录:
  • 美国化学文摘(网络版),中国中国科技核心期刊
  • 被引量:7516