脑脂质代谢调节因子的变化:抑郁症和甲状腺功能减退动物模型的研究。

Pharmacological reports : PR Pub Date : 2022-10-01 Epub Date: 2022-08-11 DOI:10.1007/s43440-022-00395-8
Katarzyna Głombik, Jan Detka, Magdalena Kukla-Bartoszek, Alicja Maciejska, Bogusława Budziszewska
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引用次数: 2

摘要

大脑代谢紊乱被认为是抑郁症发病机制的早期变化,这些变化可能因甲状腺激素缺乏而加剧。与葡萄糖代谢相反,脑脂质改变与抑郁症发病机制之间的联系尚不清楚,因此在本研究中,我们在抑郁症、甲状腺功能减退症和这些疾病共存的动物模型中确定了调节大脑结构中胆固醇和脂肪酸生物合成的转录因子和酶。在使用的抑郁症模型中,海马中转录因子SREBP-2活性形式的减少被证明,从而表明胆固醇生物合成减少。反过来,在甲状腺功能减退模型中,成熟SREBP-2的减少和参与胆固醇生物合成的酶的浓度都证明了额叶皮质中胆固醇生物合成的减少。低密度脂蛋白受体在额叶皮层的低表达表明,在抑郁症和甲状腺功能减退共存的模型中,胆固醇摄取受到限制。此外,SNAP-25、GLP-1R和GLP-2R水平的变化表明,在所检查的大脑结构中突触可塑性和神经保护机制受到干扰。综上所述,抑郁模型大鼠海马胆固醇合成减少可能是突触可塑性降低的原因,而抑郁和甲状腺功能减退共存模型大鼠额叶皮质LDL-R水平降低可能是焦虑和抑郁样行为的原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Changes in regulators of lipid metabolism in the brain: a study of animal models of depression and hypothyroidism.

Changes in regulators of lipid metabolism in the brain: a study of animal models of depression and hypothyroidism.

Changes in regulators of lipid metabolism in the brain: a study of animal models of depression and hypothyroidism.

Changes in regulators of lipid metabolism in the brain: a study of animal models of depression and hypothyroidism.

Metabolic disturbances in the brain are assumed to be early changes involved in the pathogenesis of depression, and these alterations may be intensified by a deficiency of thyroid hormones. In contrast to glucose metabolism, the link between altered brain lipids and the pathogenesis of depression is poorly understood, therefore in the present study, we determine transcription factors and enzymes regulating cholesterol and fatty acid biosynthesis in the brain structures in an animal model of depression, hypothyroidism and the coexistence of these diseases.In used model of depression, a decrease in the active form of the transcription factor SREBP-2 in the hippocampus was demonstrated, thus suggesting a reduction in cholesterol biosynthesis. In turn, in the hypothyroidism model, the reduction of cholesterol biosynthesis in the frontal cortex was demonstrated by both the reduction of mature SREBP-2 and the concentration of enzymes involved in cholesterol biosynthesis. The lower expression of LDL receptors in the frontal cortex indicates the restriction of cholesterol uptake into the cells in the model of coexistence of depression and hypothyroidism. Moreover, the identified changes in the levels of SNAP-25, GLP-1R and GLP-2R pointed to disturbances in synaptic plasticity and neuroprotection mechanisms in the examined brain structures.In conclusion, a reduction in cholesterol synthesis in the hippocampus in the model of depression may be the reason for the reduction of synaptic plasticity, whereas a lower level of LDL-R occurring in the frontal cortex in rats from the model of depression and hypothyroidism coexistence could be the reason of anxiogenic and depression-like behaviors.

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