丙泊酚对癫痫持续状态大鼠抑制作用的NMDA受体机制研究

目的观察丙泊酚对癫痫持续状态（SE）大鼠皮层NMDA受体亚型（2A，2B）表达的影响。方法60只SD大鼠随机分为空白对照组（BLK组）、SE组、丙泊酚50mg／kg组（PPF组）、安定10mg／kg组（DZP组）、东莨菪碱10mg／kg组（SCOP组）及MK-801（2mg／kg）组。匹鲁卡品30mg／kg诱发SE模型，待SE出现后30min，各实验组分别腹腔注射丙泊酚等药物，BLK组和SE组腹腔注射等容量0．9％氯化钠注射液。24h后每组取4只断头取脑，快速剥离皮层提取组织蛋白。采用Western Blot法观察丙泊酚对SE大鼠发作24h后皮层NR2A、NR2B亚型表达的影响。结果SE发作后24h，SE组大鼠皮层NR2A、NR2B亚型表达与BLK组相比显著增加fP〈0．05）；PPF组NR2B表达显著降低（与SE组相比，P〈0．05）；NR2A亚型表达无明显变化。MK-801（2mg／kg）可显著降低皮层NR2A、2B亚型的表达（与SE组相比，P〈0．05），但安定（10mg／kg）和东莨菪碱（10mg／kg）对NR2A和NR2B亚型表达无明显影响。结论丙泊酚可显著降低大鼠SE发作后皮层NR2B亚型表达。

Inhibitory effect of prpofol on expression of N-methyl-D-aspartate receptor in rats a status epilepticus

Objective To observe the effect of propofol on expression of N-methyl-D-aspartate receptor（NMDA） subunits 2A （NR2A） and 2B（NR2B） in cortex of rats at status epilepticus （SE）. Methods Sixty SD rats were randomly divided into blank group, SE group, propofol group （50mg/kg）, diazepam group （10mg/kg）, scopolamine group （10mg/kg） and MK-801 group （2mg/kg）, 10 rats in each group. A rat SE model was induced by pilocarpine （30mg/kg）. Thirty minutes after occurrence of SE, each agent was injected into the abdominal cavity of rats in different experimental groups, and an equal volume of 0.9% sodium chloride injection was injected into the abdominal cavity of rats in blank and SE groups. Twenty-four hours later, 4 rats from each group were killed with their brain collected. Tissue protein was isolated from the brain. Effect of propofol on expression of NMDA NR2A and NR2B in cortex of rats was detected 24h after SE attack. Results Twenty-four hours after SE attack, the expression level of NR2A and NR2B was significantly higher in SE group than in blank group （P〈0.05）. However, the expression level of NR2B was significantly lower in propofol group than in SE group （P〈0.05）. No difference was found in expression of NR2A between the two groups. The expression level of NR2A and NR2B was significantly lower in MK801 group than in SE group （P〈0.05）. Conclusion Propofol can significantly inhibit the expression of NR2B in cortex of rats after SE attack.