摘要
目的研究脑出血后的脑水肿形成与水孔蛋白4(AQP4)mRNA表达的关系,以及水蛭素、尼膜同的干预作用。方法采用自体动脉血注入法制作大鼠脑出血模型,RT-PCR法检测AQP4mRNA表达,并分别观察给与水蛭素、尼膜同后脑水肿(脑含水量)的变化。结果与对照组相比,脑出血组、水蛭素组及尼膜同组均从脑出血后6h开始出现脑水肿(P<0.05),3d时达到高峰(P<0.05),分别上升到(82.13±0.36)、(79.48±0.46)及(81.26±0.42),且水蛭素、尼膜同组脑水肿低于脑出血组(P<0.05);AQP4mRNA表达同样在3d时达到高峰(P<0.05),分别为(1.34±0.14)、(1.03±0.05)及(1.27±0.14)。脑水肿程度与AQP4mRNA表达的变化呈显著正相关(r=0.815,P<0.01)。结论脑出血后AQP4mRNA表达明显增加,提示AQP4参与了脑水肿的发生发展过程,而水蛭素、尼膜同能够抑制脑水肿的形成。
[Objective] Study the relationship between the cerebral edema after cerebral hemorrhage and AQP4mRNA expression, and the interferent effect of hirudin and nimotop. [Methods] The ICH models were established by stereotaxic injecting of auto-non-anticoagulated artery blood into the caudate nucleus, detected AQP4mRNA expression by RT-PCR, and cerebral edema（cerebral water contents） after giving hirudin and nimotop. [Result] Compared with the controlled group, cerebral edema appeared in ICH group, hirudin group and nimotop group 6 h after cerebral hemorrhage （P 〈0.05）, it reached peak at 3 d （P 〈0.05）, increased to （82.13±0.36）, （79.48±0.46） and （81.26±0.42） respectively, and cerebral edema of hirodin group, nimotop group were lower than cerebral hemorrhage group （P 〈0.05）. AQP4mRNA expression reached peak at 3 d （P 〈0.05）, and the levels were （1.34±0.14）, （1.03±0.05） and （1.27±0.14） respectively. There was a significantly positive correlation between BBB permeability and AQP4mRNA. [Conclusions] AQP4mRNA expression increased significantly after cerebral hemorrhage, which suggested APQ4mRNA involved in pathogenesis and development of cerebral edema, and hirudin, nimotop could inhibit cerebral edema.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2006年第9期1290-1293,共4页
China Journal of Modern Medicine
