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作 者:杜森[1] 叶琳[1] 朱琳[1] 李阳阳[1] 夏春波[1]
机构地区:[1]桂林医学院人体解剖学教研室,广西桂林541004
出 处:《中国现代医学杂志》2016年第12期1-5,共5页China Journal of Modern Medicine
基 金:国家自然科学基金资助项目(No:81260137)
摘 要:目的探讨大鼠认知障碍对糖代谢的影响及其与肝脏和骨骼肌;糖原合成酶激酶-3β(GSK-3β)表达的关系,为糖代谢的神经调节机制研究提供新的实验依据。方法 Aβ1-42大鼠海马内注射构建认知障碍模型,血糖仪检测大鼠空腹血糖(FPG),半定量反转录-聚合酶链反应法(RT-PCR)检测肝脏与骨骼肌GSK-3βmR NA的表达,蛋白印迹法(Western blot)检测肝脏与骨骼肌GSK-3β的表达。结果①实验组大鼠FPG为(7.99±0.15)mmol/L,与假手术组和对照组比较显著升高(P<0.05)。②实验组大鼠肝脏和骨骼肌GSK-3βmR NA表达水平分别为(0.47±0.03)和(0.26±0.02),与假手术组和对照组比较均明显升高(P<0.05)。③实验组大鼠肝脏和骨骼肌GSK-3β表达水平分别为(0.47±0.04)和(0.26±0.03),均显著高于假手术组与对照组(P<0.05)。结论大鼠认知障碍可引起血糖水平的升高,其机制可能与认知障碍大鼠肝脏和骨骼肌GSK-3β表达升高有关。Objective To investigate the effects of cognitive impairment in rats on glucose metabolism and its relation with the expression of GSK-3β in liver and skeletal muscle, and to provide a new experimental evidence for study of the neural mechanisms regulating glucose metabolism. Methods The Aβ1-42 was injected into the hippocampus to build cognitive impairment model of rats, and fasting blood glucose of rats was tested by blood glu- cose meter. Expression of GSK-3βmRNA and GSK-3β in liver and skeletal muscle were detected by RT-PCR and Western blot, respectively. Results In the experimental group, fasting blood glucose (FPG) was (7.99 ± 0.15) mmol/L, which was significantly higher than that in the sham group and the control group (P 〈 0.05). The expressions of GSK-3β mRNA in liver and skeletal muscle of the experimental group were (0.47±0.03) and (0.26±0.02), which were significantly higher than other two groups (P 〈 0.05). The expressions of GSK-3β in liver and skeletal muscle of the experimental group were (0.47± 0.04) and (0.26± 0.03), which also higher than other groups significantly (P 〈 0.05). Conclusions Cognitive impairment in rats causes the elevation of glucose levels, which mechanism may related to the increase of expression of GSK-3β in liver and skeletal muscle.
关 键 词:认知功能障碍 糖代谢 糖原合成酶激酶-3Β
分 类 号:R338.26[医药卫生—人体生理学]
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