【摘要】 目的研究七氟烷对新生大鼠海马Bcl-2表达的影响,探讨其在神经细胞凋亡过程中的作用机制及相互作用方式。方法7日龄健康SD大鼠24只,体质量10~14g,雌雄不拘,使用随机数字表法将实验动物随机分为两组(n=12):A组为七氟烷组,B组为吸氧对照组。将A组急性暴露于2.3%七氟烷4h。暴露结束后等候4h。从两组大鼠中各取六只处死,取海马组织,用流式细胞术检测海马神经元凋亡,免疫印迹(Western Blot)法半定量检测Bcl-2的表达。剩余的12只饲养二周后做跳台试验。结果与吸氧对照组相比,七氟烷组海马神经元凋亡显著增加(P<0.05)。Western印迹法结果显示,七氟烷组Bcl-2表达降低。跳台试验证实大鼠学习记忆能力下降。结论七氟烷急性暴露可致发育中神经元的凋亡,导致认知功能障碍,其机制可能与Bcl-2信号通路有关。更多还原

【Abstract】 Objective To study the influence of sevoflurane on the expression of hippocampal Bcl-2of new-born rat,and explore its mechanisms of action and interaction in the process of neuronal apoptosis.Methods the experiment wss performed in 24 7-day-old SD healthy female or male rats weighing 10-14g,which were randomly divided into two groups which were group A(n=12)was sevoflurane group,and group B was oxygen control group.Group A was acute-exposed to 2.3%sevoflurane for 4hours.Wait for 4hours after the exposure.The two groups of rats were sacrificed,and the hippocampal tissue was taken.FCM was applied to detect the hippocampal neuronal apoptosis,and Western Blot was used for the semi-quantitative detection of Bcl-2expression.After two weeks feeding,the rest of 12rats would done the step down test.Results compared with oxygen control group,hippocampal neuronal apoptosis was significantly increased in sevoflurane group and there were statistical significantly differences(P<0.05).The results of Western Blot was shown that in Group A,the expression of Bcl-2decreases.Step down test confirmed that the learning and memorizing ability decline. Conclusion The acute exposure to sevoflurane can cause developing neuronal apoptosis,which leads to cognitive dysfunction,whose mechanism may be related to the signaling pathway of Bc1-2.更多还原