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作 者:李海涛[1] 李中秋[1] 李玉明[1] LI Haitao;LI Zhongqiu;LI Yuming(Yanjing Medical College of Capital Medical University,,Beijing 101300,China)
机构地区:[1]首都医科大学燕京医学院机能学教研室,北京市101300
出 处:《河北医药》2018年第17期2565-2568,共4页Hebei Medical Journal
基 金:国家自然科学基金面上项目(编号:81271165);北京市自然科学基金面上项目(编号:7142019);首都医科大学燕京医学院启动基金资助(编号:20130011);首都医科大学生科研创新项目(编号:xsky2014054)
摘 要:目的探讨异丙酚减轻缺血-再灌脑组织损伤过程中钙依赖性蛋白激酶(CaMKⅡ)的作用机制。方法随机将24只小鼠分为对照组(缺血-再灌注损伤,C组)和实验组(缺血-再灌注+异丙酚干预,P组),每组12只,结合TTC染色、神经学评分、免疫印迹和免疫组化技术,观察异丙酚对缺血-再灌脑组织的保护作用,检测缺血-再灌过程中脑组织CaMKⅡ蛋白表达量和磷酸化水平。结果与对照组比较,实验组梗死面积、梗死体积和神经学评分明显减少(P<0.05);缺血-再灌区脑组织CaMKⅡ蛋白表达量和磷酸化水平均显著降低(P<0.05);脑组织切片缺血-再灌区CaMKⅡ光密度也明显降低(P<0.05)。结论异丙酚可以减轻小鼠缺血-再灌脑组织损伤,而这一作用可能与异丙酚抑制CaMKⅡ蛋白表达与磷酸化水平有关。Objective To investigate the effects and action mechanism of CaMKⅡduring propofol in relieving brain injury caused by ischemia reperfusion in mice. Methods Twenty-four mice were randomly divided into control group( n = 12)and experimental group( n = 12). The mice in control group underwent ischemia-reperfusion injury,however,the mice in experimental group were treated by propofol after ischemia-reperfusion injury. The protective effects of propofol on cerebral tissues after ischemia-reperfusion injury were evaluated by TTC staining,neurological scoring,Western Blot and immunohistochemistry,moreover,the levels of CaMK Ⅱ protein expression and phosphorylation were detected. Results As compared with those in control group,the cerebral infarction area and neurological scores experimental group were significantly decreased( P 〈 0. 05),and the levels of CaMK Ⅱ protein expression and phosphorylation of CaMKII of cerebral tissues in ischemia-reperfusion region were significantly decreased( P 〈 0. 05). Moreover the optical density of CaMKⅡ in ischemiareperfusion region was significantly reduced( P 〈 0. 05). Conclusion Propofol can relieve brain tissue injury caused by ischemia reperfusion in mice,and its action may be related to the effects of propofol in inhibiting CaMKⅡ protein expression and phosphorylation.
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