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引用本文:陶红蕾,周程,王玉慧,姜云峰,谢玉波.丙泊酚复合皮质酮对大鼠海马pCaMKⅡ表达的影响[J].中国现代应用药学,2014,31(4):409-412.
TAO Honglei,ZHOU Cheng,WANG Yuhui,JIANG Yunfeng,XIE Yubo.Combined Effects of Propofol and Corticosterone on the Expression of Phosphorylated Ca2+/ Calmodulin-dependent Protein Kinase Ⅱ in Hippocampus Region of Rats[J].Chin J Mod Appl Pharm(中国现代应用药学),2014,31(4):409-412.
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丙泊酚复合皮质酮对大鼠海马pCaMKⅡ表达的影响
陶红蕾1, 周程1, 王玉慧1, 姜云峰1, 谢玉波2
1.浙江省立同德医院麻醉科,杭州 310012;2.广西医科大学第一附属医院科研部,南宁 530021
摘要:
目的 探讨丙泊酚复合皮质酮对大鼠海马神经元Ca2+/钙调蛋白依赖性蛋白激酶Ⅱ(calcium/calmodulin dependent kinase Ⅱ,pCaMKⅡ)表达水平及细胞超微结构的影响。方法 36只21 d龄Wistar大鼠随机分为正常对照组、丙泊酚组、丙泊酚+皮质酮组3组,分别以生理盐10 mL·kg-1、丙泊酚100 mg·kg-1、丙泊酚100 mg·kg-1+皮质酮10 mg·kg-1进行腹腔注射,连续用药8 d,每组随机取6只以免疫组织化学法检测大鼠海马CA1区pCaMKⅡ的表达水平,取其余大鼠的海马组织制备透射电镜超薄切片以观察海马神经元超微结构变化。结果 与正常对照组相比较,丙泊酚组和丙泊酚+皮质酮组2组大鼠海马CA1区神经元的pCaMKⅡ表达水平明显降低(P<0.05);与丙泊酚组相比较,丙泊酚+皮质酮组pCaMKⅡ的表达更低(P<0.05)。电镜分析表明,丙泊酚组和丙泊酚+皮质酮组2组大鼠的海马神经元及细胞器发生了不同程度的改变。结论 连续8 d使用100 mg·kg-1丙泊酚,大鼠海马CA1区神经元pCaMKⅡ的表达下调;丙泊酚复合皮质酮进一步抑制pCaMKⅡ的表达,损伤大鼠海马神经元结构。
关键词:  丙泊酚  皮质酮  CaMKⅡ
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Combined Effects of Propofol and Corticosterone on the Expression of Phosphorylated Ca2+/ Calmodulin-dependent Protein Kinase Ⅱ in Hippocampus Region of Rats
TAO Honglei1, ZHOU Cheng1, WANG Yuhui1, JIANG Yunfeng1, XIE Yubo2
1.Department of Anesthesiology, Tongde Hospital of Zhejiang Province, Hangzhou, 310012;2.Department of Scientific Research, The first Affiliated Hospital of Guangxi Medical University, Nanning 530021, China
Abstract:
OBJECTIVE To investigate the effects of propofol and corticosterone on the expression of phosphorylated Ca2+/calmodulin-dependent protein kinaseⅡ(pCaMKⅡ) and cellular structure in hippocampal CA1 region. METHODS Thirty-six Wistar rats (21-day-old) were randomly divided into 3 groups: control group; propofol group; propofol+corticosterone group. Rats were received intraperitoneal injection of 10 mL·kg-1 normal saline, 100 mg·kg-1 propofol or 100 mg·kg-1 propofol+ 10 mg·kg-1 corticosterone for 8 consecutive days, respectively. In each group, six rats were selected at random for detection of the expression of pCaMKⅡ in hippocampal CA1 area by immunohistochemical assay and the rest were used to observe the neuronal ultrastructure with transmission electron microscope. RESULTS The expression of pCaMKⅡ in hippcampal CA1 neurons was significantly down-regulated in propofol group and propofol+corticosterone group, compared with that in control group. Electronic microscopic analysis showed that the ultrastructural of hippocampal neurons were damaged in both propofol group and propofol+corticosterone group. CONCLUSION Repeated propofol administration can reduce the expression of pCaMKⅡ, damage the structure of neurons. The combined application of propofol and corticosterone aggravates this effect.
Key words:  propofol  corticosterone  Ca2+/calmodulin-dependent protein kinase-Ⅱ
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