中文摘要：

目的：探讨慢性强迫游泳运动对大鼠放射性认知功能障碍是否有改善作用及其相关机制。方法将39只1月龄SD大鼠按随机数字表法分成对照组（ C）、对照游泳组（ C-S）、照射组（ R）和照射游泳组（ R-S）。照射组给予单次20 Gy全脑照射，游泳组进行15 min/d，5 d/周的强迫游泳运动。照射后第3个月依次进行自发活动、Morris水迷宫（定向航行、空间探索）行为学检测，完成后取大鼠海马组织，用Western blot方法测定各组大鼠海马中脑源性神经营养因子（ BDNF）、磷酸化细胞外调节蛋白激酶（ P-ERK）、总细胞外调节蛋白激酶（ T-ERK）、磷酸化的环磷腺苷效应元件结合蛋白（ P-CREB）和总环磷腺苷效应元件结合蛋白（ T-CREB）的分子水平。结果 Morris水迷宫定向航行实验中，对照游泳组第2天平均潜伏期低于对照组，对照组及照射游泳组第2天平均潜伏期低于照射组（ P＜0？05）。自发活动、Morris水迷宫空间探索实验各组之间差异无统计学意义（ P ＞0？05）。 Western blot检测，与对照组比较，电离辐射显著降低了BDNF及其下游信号分子P-ERK和P-CREB的表达（P＜0？05），但是强迫游泳运动改善了这种情形，显著提高了照射组BDNF及其下游信号分子P-ERK和P-CREB的表达（P＜0？05）。结论慢性强迫游泳运动可改善大鼠放射性认知功能障碍，其机制可能是促进海马内BDNF及其下游信号分子P-ERK和P-CREB的表达。

英文摘要：

Objective To explore whether chronic forced swimming stress could improve whole brain radiation induced cognitive dysfunction and possible mechanism. Methods Thirty-nine one month old male Sprague-Dawley rats were randomized into sham control group （ C ） , swimming group （ C-S ） , radiation group（ R） , and radiation plus swimming group（ R-S） . Radiation groups were given a single dose of 20 Gy on whole-brain. Rats in the swimming groups were trained with swimming of 15 min/d, 5 d/w. Rat behavior was performed 3 months after radiation in an order of free activity in an open field and the Morris water maze test including the place navigation and spatial probe tests. Then, the protein expressions of BDNF, P-ERK, T-ERK, P-CREB and T-CREB in the rat hippocampus tissue were assayed by Western blot. Results On the day 2, in the place navigation test of Morris water maze, the latency of swimming group was significantly shorter than that of sham group, the latency of sham group was significantly shorter than that of radiation group, and the latency of radiation swimming group was significantly shorter than that of radiation group（P〈0？05）. In the open field test, the latencies of the place navigation and spatial probe tests of Morris water maze had no significant difference among four groups （P〉0？05）. Western blot assay showed that the expressions of BDNF and its downstream signals including P-ERK and P-CREB were markedly reduced by radiation （ P 〈 0？05 ） , but this reduction was attenuated by the chronic forced swimming stress. Conclusion The chronic forced swimming stress could improve whole brain radiation induced cognitive dysfunction by up-regulating the expressions of BDNF and its downstream signal molecules of P-ERK and P-CREB in hippocampus.