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Proteomic analysis reveals energy metabolic dysfunction and neurogenesis in the prefrontal cortex of a lipopolysaccharide-induced mouse model of depression

机译:蛋白质组学分析揭示了脂多糖诱导的抑郁症小鼠模型的前额叶皮层能量代谢功能障碍和神经发生

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Substantial evidence from previous studies has suggested an association between major depressive disorder (MDD) and inflammation, and previous studies have associated prefrontal cortex (PFC) dysfunction with MDD. Systemic administration of bacterial lipopolysaccharide has been used to study inflammation-associated behavioral changes in rodents. However, proteomic studies investigating PFC protein expression in an LPS-induced mouse model of depression have yet to be conducted. Using two-dimensional electrophoresis coupled with matrix-assisted laser desorption ionization-time of flight-tandem mass spectrometry, PFC proteomes were comparatively assessed in LPS-induced acute inflammation reaction mice, LPS-induced depressive-like behavior mice (Dep), and control mice. A total of 26 differentially expressed proteins were identified, two of which were selected for western blot analysis, the results of which revealed a significant increase in the expression levels of creatine kinase B and dihydropyrimidinase-like 3 in Dep mice, suggesting that changes in energy metabolism and neuro-genesis occur in the PFC of Dep mice. Further investigation on these processes and on the proteins of the PFC are required in order to elucidate the pathophysiological mechanism underlying MDD.
机译:先前研究的大量证据表明,严重抑郁症(MDD)与炎症之间存在关联,并且先前的研究将前额叶皮质(PFC)功能障碍与MDD相关。细菌脂多糖的全身给药已被用于研究啮齿动物中与炎症相关的行为变化。但是,尚未进行蛋白质组学研究,以研究LPS诱导的小鼠抑郁模型中PFC蛋白的表达。使用二维电泳结合基质辅助激光解吸电离飞行时间质谱,在LPS诱导的急性炎症反应小鼠,LPS诱导的抑郁样行为小鼠(Dep)和对照中比较了PFC蛋白质组老鼠。总共鉴定出26种差异表达的蛋白质,其中两种选择用于蛋白质印迹分析,其结果显示Dep小鼠中的肌酸激酶B和二氢嘧啶酶样3的表达水平显着增加,表明能量的变化代谢和神经发生发生在Dep小鼠的PFC中。为了阐明MDD的病理生理机制,需要对这些过程和PFC的蛋白质进行进一步的研究。

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