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作 者:马文群[1] 李胜超[2] 张金霞[1] 孙国柱[3]
机构地区:[1]河北省邯郸市中心医院神经外科,056001 [2]河北医科大学第四医院肝胆外科 [3]河北医科大学第二医院神经外科
出 处:《中华实验外科杂志》2013年第9期1838-1840,共3页Chinese Journal of Experimental Surgery
基 金:河北省自然科学基金资助项目(C2008001084);河北省科技厅资助项目(08206123D);河北省卫生厅资助课题项目(20120073)
摘 要:目的 观察大鼠颅脑液压冲击伤后水肿脑组织水通道蛋白4(AQP4)蛋白及其mRNA的表达变化.方法 成年雄性SD大鼠64只,应用Dixon法制作颅脑损伤模型,术后6、12、24 h、3、7d用干湿重法、免疫组织化学法、Western blot以及逆转录-聚合酶链反应(RT-PCR)分别测定水肿脑组织含水量、AQP4蛋白及其mRNA的表达.结果 自伤后6h,脑组织含水量开始增加(79.11±1.28)%,24 h达高峰[(82.74±1.10)%],持续至3 d[(82.04±1.69)%],然后开始下降.组织学观察印证了脑组织的水肿趋势.AQP4于伤后6h开始增加[积分吸光度(IA)值为471.40±45.19],24 h达高峰(IA值为944.20±101.84),持续至3d后下降(IA值为920.60±194.22),7d仍高于对照组;而AQP4 mRNA表达变化趋势与其蛋白含量变化一致.线性相关分析可见AQP4蛋白及其mRNA表达与脑含水量呈正相关(rp=0.981;rm =0.973,P<0.05).结论 AQP4表达上调在液压冲击伤性脑水肿演变中起重要作用.Objective To investigate the expression of apuaporin 4 (AQP4) protein and mRNA in cerebral edema following fluid percussion injury in rats.Methods The experimental models were established in 64 rats according to Dixon's method.The water content of injured brain and the expression of AQP4 protein and mRNA were measured by using dry-wet measure,immunohistochemistry,Western blotting and reverse transcriptase-polymerase chain reaction (RT-PCR) at 1st h,6th h,12th h,24th h,3rd day and 7th day after operation respectively.Results As compared with control group,the water content was increased in model group from 6 h [(79.11 ± 1.28) %],reached the peak at 24 h [(82.74 ±1.10)%],lasted to 3rd day [(82.04 ± 1.69)%],and then began to drop; the AQP4 expression was increased from 6 h (IA 471.40 ±45.19),reached the maximum at 24 h (IA 944.20 ± 101.84),lasted to 3rd day (IA 920.60 ± 194.22) and began to drop.Until 7th day,the AQP4 immunoreactive expression was still higher in model group than in control group.The linear regression analysis indicated that the expression of AQP4 protein and mRNA in edematous brain had a positive correlation with change of brain water content (rp,=0.981 ;rm =0.973,P < 0.05).Conclusion The AQP4 expression upregulation plays an important role in cerebral edema following fluid percussion injury in rats and inhibition of AQP4 upregulation may become the new strategy for treatment of traumatic brain edema.
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