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作 者:林季[1] 颜光涛[1] 郝秀华[1] 张凯[1] 王录焕[1] 薛辉[1]
机构地区:[1]解放军总医院基础医学研究所生化研究室,北京100853
出 处:《四川大学学报(医学版)》2006年第4期574-577,共4页Journal of Sichuan University(Medical Sciences)
基 金:国家自然科学基金(批准号39970717)资助
摘 要:目的研究肠缺血/再灌注(I/R)损伤对血浆及下丘脑O rex in-A水平的影响,探讨O rex in-A在急性炎症反应中的作用。方法建立大鼠肠I/R损伤模型,设立缺血60 m in后不同时间的再灌注损伤组。采用放射免疫分析法测量血浆及下丘脑O rex in-A的蛋白水平,采用RT-PCR检测下丘脑O rex in-A的mRNA表达水平。结果与损伤前自身对照相比,各组损伤后的血浆O rex in-A水平无明显变化(P>0.05);与损伤后假手术组相比,其他各组损伤后的血浆或下丘脑O rex in-A蛋白水平亦无明显变化(P>0.05);与损伤后假手术组下丘脑O rex in-A mRNA表达水平相比,肠缺血60 m in/再灌注30 m in(I60′R 30′)组、I60′R 90′组逐步降低,I60′R 150′组最低,I60′R 240′组、I60′R 360′组逐步回升但仍低于假手术组。结论O rex in-A对肠I/R损伤具有迟缓的应答效应,可能在急性炎症损伤所致的代谢障碍中发挥一定的炎症因子作用。Objective To investigate the effect of intestinal ischemia/reperfusion (I/R) injury on orexin-A levels in plasma and hypothalamus, and to find out the role of orexin-A in acute inflammatory responses. Methods Fifty-four SD rats were randomly divided into a sham-operation group and 5 experiment groups. Then we established the intestinal I/R injury model of rats and setup the 5 experiment groups of 60 min ischemia followed by different periods of time for reperfusion. Protein levels of orexin-A in plasma and hypothalamus were measured by radioimmunoassay, and the changes of orexin-A mRNA expression in hypothalamus were detected by RT-PCR. Results By analyses on the orexin-A levels in plasma of rats before and after injury, no significant change was observed in the 5 experiment groups (P〉0.05), and the 5 groups' post-injury orexin-A levels in plasma and hypothalamus were not significantly different from the sham-operation group's (P〉0.05). However, by comparison with the sham-operation group after injury, the experiment groups were found to have orexin-A mRNA levels in hypothalamus significantly decreased step by step from 60 min ishchemia/30 min reperfusion (I60'R30') to I60'R150'; the lowest level was seen at I60'R150'; and at I60'R240' and I60'R360', the level recovered slowly, but it was still lower than that seen in the sham-operation group. Conclusion Orexin-A makes a delayed response to intestinal I/R injury and may function as inflammatory cytokine in the metabolic disorders caused by acute inflammation.
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