首页> 外文期刊>Clinical and experimental pharmacology & physiology >Chronic consumption of a high-fat diet rich in corn oil activates intrinsic cell death pathway and induces several ultrastructural changes in the atria of healthy and type 1 diabetic rat
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Chronic consumption of a high-fat diet rich in corn oil activates intrinsic cell death pathway and induces several ultrastructural changes in the atria of healthy and type 1 diabetic rat

机译:富含玉米油脂的高脂肪饮食的慢性消耗激活内在细胞死亡途径,并在健康和1型糖尿病大鼠的Atria诱导几种超微结构变化

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This study investigates the effect of chronic consumption of a high-fat diet rich in corn oil (CO-HFD) on atrial cells ultrastructure, antioxidant levels and markers of intrinsic cell death of both control and type 1 diabetes mellitus (T1DM)-induced rats. Adult male rats (10 rats/group) were divided into four groups: control fed standard diet (STD) (3.82 kcal/g, 9.4% fat), CO-HFD (5.4 kcal/g, 40% fat), T1DM fed STD, and T1DM + CO-HFD. CO-HFD and T1DM alone or in combination impaired systolic and diastolic functions of rats and significantly reduced levels of GSH and the activity of SOD, enhanced lipid peroxidation, increased protein levels of P53, Bax, cleaved caspase-3, and ANF and decreased levels of Bcl-2 in their atria. Concomitantly, atrial cells exhibited fragmentation of the myofibrils, disorganized mitochondria, decreased number of atrionatriuretic factor (ANF) granules, and loss of gap junctions accompanied by changes in capillary walls. Among all treatments, the severity of all these findings was more severe in T1DM and most profound in the atria of T1DM + CO-HFD. In conclusion, chronic consumption of CO-HFD by T1DM-induced rats elicits significant biochemical and ultrastructural damage to rat atrial cells accompanied by elevated oxidative stress and mitochondria-mediated cell death.
机译:本研究研究了富含玉米油(CO-HFD)的高脂肪饮食慢性消费对心房细胞超微结构,抗氧化水平和对照组的抗氧化水平和标志物的影响,对照组和1型糖尿病(T1DM)诱导的大鼠。成年雄性大鼠(10只大鼠/组)分为四组:控制喂养标准饮食(STD)(3.82千卡/克,9.4%脂肪),Co-HFD(5.4千卡/克,40%脂肪),T1DM喂养STD和T1DM + CO-HFD。单独的CO-HFD和T1DM单独或组合的收缩性和舒张功能的大鼠的舒张功能和GSH水平显着降低以及SOD的活性,增强的脂质过氧化,P53,BAX,切割的caspase-3和ANF的蛋白质水平增加,抗植物水平和ANF降低Bcl-2在他们的阿里亚。伴随着,心房细胞表现出肌原纤维的破碎化,杂皮病的破坏性线粒体,减少的含有尿剂因子(ANF)颗粒的数量,并且伴随毛细血管壁的变化伴随着间隙连接的损失。在所有治疗中,所有这些发现的严重程度在T1DM中更严重,在T1DM + Co-HFD的Atria中最深刻。总之,T1DM诱导的大鼠Co-HFD的慢性消耗引发了大鼠心房细胞的显着生化和超微结构损伤,伴随着氧化应激和线粒体介导的细胞死亡。

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