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丙咪嗪、帕罗西汀和碳酸锂对链脲佐菌素诱导的大鼠神经行为变化的影响:对糖原合酶激酶-3和血糖水平的影响

Effect of Imipramine, Paroxetine, and Lithium Carbonate on Neurobehavioral Changes of Streptozotocin in Rats: Impact on Glycogen Synthase Kinase-3 and Blood Glucose Level.

作者信息

Nadeem Rania I, Ahmed Hebatalla I, El-Denshary Ezz-El-Din S

机构信息

, Cairo, Egypt.

出版信息

Neurochem Res. 2015 Sep;40(9):1810-8. doi: 10.1007/s11064-015-1670-6. Epub 2015 Jul 28.

Abstract

Recent studies have demonstrated a scrutinized association of diabetes mellitus with depressive symptoms and major depression. Glycogen synthase kinase-3 (GSK-3) is a protein kinase enzyme constitutively active in non-stimulated cells and in multiple signalings. Independent lines of research provide a converging evidence for an involvement of GSK-3 in the regulation of behavior and hyperglycemia. The present study revealed that streptozotocin (STZ)-induced diabetic rats were found to show lengthened duration of immobility in the forced-swimming test (FST) and reduced locomotor and exploratory activities in the open-field test (OFT). Imipramine (15 mg/kg), Paroxetine (10 mg/kg) and lithium carbonate (36.94 mg/kg) for 14 days reduced immobility behavior in FST. Paroxetine and lithium carbonate increased the locomotor and exploratory activities, while imipramine decreased the locomotor activity in the OFT. Imipramine and lithium carbonate reduced the blood glucose level while paroxetine didn't alter it. STZ-induced diabetes increased GSK-3 gene expression which was determined using the reverse transcription-quantitative polymerase chain reaction test, while the three drugs decreased its expression. It can be concluded that lithium carbonate and imipramine can control both hyperglycemia and the associated symptoms of depression at the same time by inhibiting GSK-3 activity. On the other hand, paroxetine may only manage the depressive-like symptoms associated with diabetes through modulating the enzyme GSK-3, without changing blood glucose levels.

摘要

最近的研究表明,糖尿病与抑郁症状及重度抑郁症之间存在密切关联。糖原合酶激酶-3(GSK-3)是一种蛋白激酶,在未受刺激的细胞及多种信号传导中持续活跃。多项独立研究表明,GSK-3参与行为调节及高血糖的过程。本研究发现,链脲佐菌素(STZ)诱导的糖尿病大鼠在强迫游泳试验(FST)中静止不动的时间延长,在旷场试验(OFT)中的运动和探索活动减少。给予丙咪嗪(15毫克/千克)、帕罗西汀(10毫克/千克)和碳酸锂(36.94毫克/千克)14天可减少FST中的静止不动行为。帕罗西汀和碳酸锂增加了运动和探索活动,而丙咪嗪在OFT中降低了运动活动。丙咪嗪和碳酸锂降低了血糖水平,而帕罗西汀未改变血糖水平。使用逆转录-定量聚合酶链反应试验测定,STZ诱导的糖尿病增加了GSK-3基因表达,而这三种药物降低了其表达。可以得出结论,碳酸锂和丙咪嗪可通过抑制GSK-3活性同时控制高血糖及相关抑郁症状。另一方面,帕罗西汀可能仅通过调节GSK-3酶来控制与糖尿病相关的抑郁样症状,而不改变血糖水平。

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