中文摘要：

目的探讨新生期大鼠反复长程惊厥对其神经行为和海马凋亡／自噬蛋白B细胞淋巴瘤／白血病基因-2（Bcl-2）、Beclin-1和可塑性相关基因-1（PRG-1）表达的远期影响及泡泡浴的干预效果。方法采用随机数字表法将日龄6d的SD大鼠分成对照组、水疗对照组、惊厥组及惊厥水疗组，每组15只。将惊厥组及惊厥水疗组大鼠置于实验舱中，并给予三氟乙醚吸人诱导其惊厥发作，持续30min，连续作用6d；对照组及水疗对照组大鼠亦于相同时间点置于实验舱内，但未给予三氟乙醚吸人。于末次惊厥后次日给予惊厥水疗组及水疗对照组泡泡浴干预，持续28d。4组大鼠于出生后第26天进行旷场实验，于出生后第43～49天进行Morris水迷宫测试，于出生后第50天处死并提取海马组织，采用免疫印迹技术检测各组大鼠海马Bcl-2、Beclinl及PRG-1表达情况。结果①惊厥组旷场得分较对照组明显降低（P〈0．05），惊厥水疗组旷场得分较惊厥组明显升高（P〈0．05）。②Morris水迷宫测试发现各组大鼠逃避潜伏期均随时间进展逐渐缩短，其中惊厥组第4，5天时逃避潜伏期较对照组明显延长（P〈0．05）；惊厥水疗组第4天时逃避潜伏期较惊厥组明显缩短（P〈0．05）。③惊厥组海马PRG-1表达较对照组明显增强（P〈0．05），惊厥水疗组PRG-1表达与惊厥组间差异无统计学意义（P〉0．05）；惊厥组海马Bcl-2表达较对照组明显降低（P〈0．05）；惊厥水疗组Bcl-2表达较惊厥组显著增强（P〈0．05）；各组大鼠Beclinl表达组间差异均无统计学意义（P〉0．05）。结论新生期反复长程惊厥对大鼠神经行为功能具有远期损害作用，其病理过程可能与上调海马PRG-1表达及下调Bcl-2表达有关；早期运动训练能够显著缓解反复惊厥所致的神经行为损伤，其治疗机制可能与上调海马Bcl-2表达有关。

英文摘要：

Objective To explore the long-term effects of bubble baths on seizure-induced neurobehavior deficits and the expression of apoptotic/autophagic marker B cell lymphoma/leukemia-2 （Bcl-2） , Beclin-1 , and plasticity-related gene-1 （PRG-1） in newborn rats. Methods Sixty rats aged 6 days were randomly divided into 4 groups： a control group （CON） , a control hydrotherapy group （HCON） , a recurrent-seizure group （RS） and a recurrent-seizure hydrotherapy group （HRS） , with 15 in each group. Flurothyl was used to induce 30 nlin of seizures daily for 6 consecutive days in the RS and HRS groups. Rats in the CON and HCON groups were placed in the same container for equal duration without exposure to flurothyl. Rats in the HCON and HRS groups were given bubble baths for 28 consecutive days after the end of the last seizure. Neurobehavioral damage was observed using open field behavior at postnatal day 26 （P26） and Morris water maze performance at postnatal day 43 to 49 （P43-P49） and a single-blind method. PRG-1, Bcl-2 and Beclin-1 protein levels in the hippocampus were detected by Western blotting at postnatal day 50 （1750）. Results ①The average open field test scores of the RS rats decreased significantly compared with those of the CON and HRS rats at P26. ②In the Morris water maze test the average latencies of all rats decreased gradually from the 1 st to 5th days （ dl to dS） after establishment of seizure model. The average escape latency was significantly longer for rats of the RS group than for CON group rats at the 4th and 5th days （ d4 and d5） after establishment of seizure model. The escape latency was significantly shorter for rats of the HRS group than for RSgroup rats at d4. ③The level of Bcl-2 protein in the hippocampus was much lower in the RS group than in the HRS and control groups. In addition, the expression of PRG-1 in the RS group was significantly higher than in the CON group. Conclusions Recurrent prolonged seizures cause long-term neurobehavior deficit