摘要
目的 评价七氟醚麻醉对幼鼠海马c．Jun氨基末端激酶（JNK）表达和神经细胞凋亡的影响。方法健康雄性sD大鼠40只，日龄30～35d，体重100～110g，采用随机数字表法，将其随机分为2组（Ⅱ=20）：对照组（c组）：吸人含有30％氧气的空氧混合气体5h；七氟醚组（s组）：吸入3％七氟醚5h，并维持麻醉箱氧浓度为30％。苏醒后1h时，每组随机处死10只大鼠，取两侧海马组织，分别采用免疫组化法和Westemblot法测定磷酸化JNK（p-JNK）的表达水平，采用TUNEL法检测神经细胞凋亡情况。苏醒后24h时，每组随机取10只大鼠，采用Morris水迷宫测试认知功能。结果与C组比较，S组海马组织p-JNK表达上调，周亡细胞计数升高，潜伏期延长和平台象限停留时间缩短（P〈0．05或0．01）。结论吸入3．0％七氟醚可能通过激活JNK信号通路，诱发海马神经细胞凋亡，从而导致幼鼠认知功能降低。
Objective To investigate the effects of sevoflttrane anesthesia on the expression of c-Jun Nterminal kinase （JNK） and neuronal apoptosis in hippocampus in juvenile rats. Methods Forty healthy male SD rats, aged 30-35 days, weighing 100-110 g, were randomly divided into 2 groups （ n = 20 each） ： control group （group C） and sevoflurane group （group S）. Group C inhaled a gas mixture of oxygen and air for 5 h and group S 3% sevoflurane for 5 h. The concentration ,ff oxygen in both groups was maintained at 30%. Ten rats in each group were scarified at 1 h after regaining corsciousness and the hippocampi removed for determination of phospho- JNK expression （by immuno-histochemistry and Western blot） and neuronal apoptosis （by TUNEL）. Another 10 rats were selected at 24 h after regaining consciousness to assess the cognitive function using Morris water maze. Results Compared with group C, phospho-JNK expression was significantly up-regulated, the number of apoptotic neurons increased, the latency prolonged and the duration of staying at the original platform quadrant shortened in group C （ P 〈 0.05 or 0101 ）. Conclusion Inhalation of 3.0% sevoflurane can induce neuronal apoptosis in hippocampus by activating JNK signaling pathway, thus leading to cognitive decline in juvenile rats.
出处
《中华麻醉学杂志》
CAS
CSCD
北大核心
2011年第5期563-565,共3页
Chinese Journal of Anesthesiology
基金
江苏省“六大人才高峰”基金（（6-B-065）
徐州市铜山区社会发展基金（TS005）
