Lin Ji, Yan Guangtao, Gao Xiaoning, Liao Jie, Hao Xiuhua, Zhang Kai
Research Laboratory of Biochemistry, General Hospital of PLA, Beijing, 100853, China.
Front Med China. 2007 Feb;1(1):87-92. doi: 10.1007/s11684-007-0017-3.
The aim of this paper is to explore the effect of intestinal ischemia/reperfusion (I/R) injury on leptin and orexin-A levels in peripheral blood and central secretory tissues, and to examine the roles of leptin and orexin-A in acute inflammatory responses. An intestinal I/R injury model of rats was made; the rats were grouped according to the time of after 60 min ischemia. Radioimmunoassay was employed to detect the levels of leptin in serum and adipose tissue and orexin-A levels in plasma and hypothalamus. Reverse transcriptase-polymerase chain reaction was used to detect mRNA expressions of adipose leptin and hypothalamus orexin-A. Compared with the levels before the injury, serum leptin in 60 min ischemia/30 min reperfusion (I60'R30') group decreased and that of I60'R360' group increased. Compared with sham-operation group (sham group) after injury, serum leptin level of I60'R360' group increased, adipose leptin levels of I60'R30' and I60'R90' decreased, and adipose leptin in I60'R360' group increased. After the injury, adipose leptin mRNA expressions of I60'R30', I60'R240' and I60'R360' increased, whereas that of I60'R150' group decreased as compared with the sham group. There was no significant difference in the protein levels of orexin-A, either between plasma and hypothalamus or between pre-and post-I/R injury. Compared with sham group, hypothalamus orexin-A mRNA expressions of I60'R30' and I60'R90' decreased gradually after the injury, with that of I60'R150' group reaching the lowest, and those of I60'R240' and I60'R360' recovering gradually, although they were still significantly lower than that of sham group. Leptin and orexin-A respond to intestinal I/R injury in a time-dependent manner, with leptin responding more quickly than orexin-A does, and both of them may contribute to the metabolic disorders in acute inflammation.
本文旨在探讨肠道缺血/再灌注(I/R)损伤对外周血及中枢分泌组织中瘦素和食欲素A水平的影响,并研究瘦素和食欲素A在急性炎症反应中的作用。制备大鼠肠道I/R损伤模型;根据缺血60分钟后的时间对大鼠进行分组。采用放射免疫分析法检测血清和脂肪组织中瘦素水平以及血浆和下丘脑中食欲素A水平。运用逆转录聚合酶链反应检测脂肪组织瘦素和下丘脑食欲素A的mRNA表达。与损伤前水平相比,60分钟缺血/30分钟再灌注(I60'R30')组血清瘦素降低,I60'R360'组血清瘦素升高。与损伤后的假手术组(假手术组)相比,I60'R360'组血清瘦素水平升高,I60'R30'和I60'R90'组脂肪组织瘦素水平降低,I60'R360'组脂肪组织瘦素升高。损伤后,I60'R30'、I60'R240'和I60'R360'组脂肪组织瘦素mRNA表达升高,而I60'R150'组与假手术组相比降低。食欲素A的蛋白水平在血浆和下丘脑之间以及I/R损伤前后均无显著差异。与假手术组相比,I60'R30'和I60'R90'组损伤后下丘脑食欲素A的mRNA表达逐渐降低,I60'R150'组降至最低,I60'R240'和I60'R360'组逐渐恢复,尽管仍显著低于假手术组。瘦素和食欲素A对肠道I/R损伤呈时间依赖性反应,瘦素比食欲素A反应更快,二者均可能导致急性炎症中的代谢紊乱。