手术创伤对老龄大鼠认知功能及海马铁调素和膜铁转运蛋白1表达的影响

Effect of surgical trauma on cognitive function and expression of hepcidin and ferroportin 1 in hippocampus in aged rats

目的评价手术创伤对老龄大鼠认知功能及海马铁调素和膜铁转运蛋白1（FP1）表达的影响。方法健康老龄雄性sD大鼠100只，18月龄，体重400～500g，采用随机数字表法，将其分为2组（n=50）：对照组（C组）腹腔注射水合氯醛麻醉，但不进行手术；手术创伤组（ST组）腹腔注射水合氯醛麻醉后行改良性剖腹探查术30min。于术后24h时随机取10只大鼠，行水迷宫实验，测定认知功能，持续6d，分别于水迷宫实验第1、3、5、7天时随机取10只大鼠处死，取脑，分离海马，采用PCR和Westernblot法检测海马铁调素和FP1的表达。结果与C组比较，ST组水迷宫实验第3、4、5天时大鼠逃避潜伏期延长，原平台象限停留时间缩短，穿越原平台次数减少（P〈0．05），各时点海马铁调素表达上调，FP1表达下调（P〈0．05）。结论手术创伤可降低老龄大鼠认知功能，其机制可能与上调海马铁调素表达，下调FP1表达有关。

Objective To evaluate the effect of surgical trauma on the cognitive function and expression of hepcidin and ferroportin 1 （FP1） in hippocampus in aged rats. Methods One hundred male Sprague-Dawley rats, aged 18 months, weighing 400-500 g, were randomly divided into 2 groups with 50 rats in each group： control group （group C） and surgical trauma group （group ST）. The rats were anesthetized with chloral hydrate, but un- derwent no operation in group C. The rats were anesthetized with chloral hydrate and underwent 30 min of modified exploratory laparotomy in group ST. Ten rats were chosen from each group at 24 h after operation and the cognitive function was assessed using Morris water-maze test for 6 consecutive days. Ten rats were sacrificed on 1st, 3rd, 5th and 7th days after beginning of Morris water-maze test and brains were removed for determination of hepcidin and FP1 expression in hippocampus by PCR and Western blot. Results Compared with group C, the escape laten- cy was significantly prolonged, the time of staying at the original platform quadrant and frequency of crossing the original platform were decreased on 3rd, 4th and 5th days after beginning of Morris water-maze test, and the ex- pression of hepcidin was up-regnlated and the expression of FP1 was down-regulated at each time point in group ST （ P 〈 0.05）. Conclusion Surgical trauma can decrease the cognitive function in aged rats and the mechanism may be related to up-regulation of hepcidin expression and down-regulation of FP1 expression in hippocampus.