High salt (HS) dietary intake leads to impaired vascular endothelium-dependent responses to various physiological stimuli, some of which are mediated by arachidonic acid (AA) metabolites. Transgenic Tff3-/- gene knockout mice (Tff3-/-/C57BL/6N) have changes in lipid metabolism which may affect vascular function and outcomes of stroke. We aimed to study the effects of one week of HS diet (4% NaCl) on vascular function and stroke induced by transient occlusion of middle cerebral artery in Tff3-/- and wild type (WT/C57BL/6N) mice. Flow-induced dilation (FID) of carotid artery was reduced in WT-HS mice, but not affected in Tff3-/--HS mice. Nitric oxide (NO) mediated FID. NO production was decreased with HS diet. On the contrary, acetylcholine-induced dilation was significantly decreased in Tff3-/- mice on both diets and WT-HS mice. HS intake and Tff3 gene depletion affected the structural components of the vessels. Proteomic analysis revealed a significant effect of Tff3 gene deficiency on HS diet-induced changes in neuronal structural proteins and acute innate immune response proteins' expression and Tff3 depletion, but HS diet did not increase the stroke volume, which is related to proteome modification and upregulation of genes involved mainly in cellular antioxidative defense. In conclusion, Tff3 depletion seems to partially impair vascular function and worsen the outcomes of stroke, which is moderately affected by HS diet.

译文

高盐 (HS) 饮食摄入导致对各种生理刺激的血管内皮依赖性反应受损,其中一些是由花生四烯酸 (AA) 代谢产物介导的。转基因Tff3-/-基因敲除小鼠 (Tff3-/C57BL/6N) 的脂质代谢变化可能会影响血管功能和中风的结局。我们旨在研究一周的HS饮食 (4% NaCl) 对Tff3-/-和野生型 (WT/C57BL/6N) 小鼠大脑中动脉短暂闭塞引起的血管功能和中风的影响。在WT-HS小鼠中,颈动脉的血流诱导扩张 (FID) 减少,但在Tff3-/-HS小鼠中不受影响。一氧化氮 (NO) 介导FID。HS饮食不会减少任何产量。相反,在饮食和WT-HS小鼠中,Tff3-/-小鼠中乙酰胆碱诱导的扩张作用均显着降低。HS摄入和Tff3基因耗竭影响血管的结构成分。蛋白质组学分析显示,Tff3基因缺乏对HS饮食诱导的神经元结构蛋白和急性先天免疫反应蛋白表达的变化以及Tff3耗竭有显着影响,但HS饮食并未增加中风量,这与蛋白质组修饰和上调主要参与细胞抗氧化防御的基因有关。总之,Tff3耗竭似乎部分损害了血管功能并恶化了中风的结局,中风受到HS饮食的适度影响。

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