摘要
目的探讨脂氧素A4（LXA4）对大鼠心肌缺血再灌注损伤（MIRI）超微结构的保护作用。方法72只SD雄性大鼠随机分成假手术一组（C、组）、假手术二组（C2组）、MIRI一组（I／R、组）、MIRI二组（I／R2组）、MIRI前用药组（LX1组）、MIRI后用药组（LX2组），每组12只。建立大鼠MIRI模型，各组于开胸前取血（T1）、实验结束后取血（T2）测IL-1β、IL-8、cTn1血清浓度；同时测定SOD活性、MDA含量；TUNEL法检测心肌细胞凋亡率；电镜下观察心肌超微结构的变化。结果1／R1、LX1、与C1组相比，I／R2、LX2与C2组相比，血清IL-1β、IL-8、cTnI浓度（均为T2），SOD、MDA以及凋亡率增高（P〈0．05）。LX1与1／R1组。LX2与I／R2组相比，血清IL-1B、IL-8、cTnI浓度（均为L），MDA含量及凋亡率均降低（均P〈0．05）；SOD活性提高（P〈0．05）；同时心肌超微结构损伤明显改善，线粒体排列整齐，电子密度增高。肿胀及空泡明显减轻。结论LXA4通过抑制组织促炎细胞因子、氧自由基损伤，降低细胞凋亡来减轻心肌超微结构的损伤，对大鼠MIRI起明显的保护作用。
Objective To investigate the protective effect of lipoxinA4 （LXA4） on myocardial ultrastructure upon ischemi- a-reperfusion injury （MIRI） in rats. Methods Seventy-two male SD rats were randomly divided into six groups with 12 in each group： sham operation groupl（group C1）, sham operation group2 （group C2）, MIRI group1 （group I/R1）, MIRI group2 （group I/R2）, pre-MIRI treatment group1 （group LX1）, post-MIRI treatment group2 （group LX2）. The rat model of MIRI was established, blood was taken in each group before chest opening（T1） and at the end of the experiment（T2）. The serum IL-1 β, IL-8, cTnl concentrations were measured and at the same time the SOD activity and MDA contents were determined, myocardial cell apoptosis was detected with TUNEL method, while the ultrastructural changes of cardiac muscle were observed under electron microscope. Results In group I/R1, LX1（compared with group C1） and group I/R2, LX2 （compared with group C2）, the serum IL-1β, IL-8, cTnl concentrations （all at T2）, SOD activity, MDA contents and the apoptotic index increased significantly （P〈0.05）. In group LX, （compared to group lIRa） and group LX2 （compared to group I/R2）, lipoxinA4 significantly reduced the serum IL-1β, IL-8, cTnl concentrations （all at T2）, the MDA contents and the apoptotic index, but increased SOD activity（P〈0.05）. At the same time, myocardial ultrastructural injury improved significantly, mitochondria arranged in rows, electron density increased, swelling and vacuolization reduced. Conclusion LXA4 has protective effect against MIRI in rats through inhibition of pro-inflammatory cytokines, oxygen free radicals and the cell apoptosis to attenuate myocardial ultrastructural injury.
出处
《浙江医学》
CAS
2013年第5期334-337,共4页
Zhejiang Medical Journal
基金
浙江省教育厅科研计划项目（Y200804950）
浙江省外科学重中之重学科开放基金资助项目（2011MZ005）
浙江省卫生厅重点支撑学科-小儿外科学基金资助项目（11-ZC27）
关键词
心肌缺血再灌注损伤
脂氧素
氧化应激
凋亡
超微结构
Myocardial ischemia-reperfusion injury Lipoxin Oxidative stress Apoptosis UItrastructure
