铁给药对大动脉铁含量和血管化在负载慢性病大鼠的作用

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Masa Nakanishi¹, Ayako Goto¹, Takahide Iwasaki²

¹Division of Kidney, Dialysis and Cardiology, Department of Internal Medicine, Hyogo Medical University, Nishinomiya, 663-8501, Hyogo, Japan.

|December 15, 2023

概括

在慢性病 (CKD) 中,铁的使用增加了大动脉铁,但没有恶化血管化 (VC). Nrf2通路的激活与铁水平相关,这表明在CKD患者的氧化应激反应中发挥了作用.

科学领域:

腎臟病學 (nephrology) 是一種醫學.
心血管医学心血管医学
生物化学生物化学

背景情况:

心血管疾病 (CVD) 是慢性病 (CKD) 患者的主要死亡原因,可能与氧化压力有关.
血管化 (VC) 是CKD中加速心血管疾病的一个关键风险因素.
(Pi),铁 (Fe) 和Nrf2是CKD中VC和氧化应激的关键调节剂.

研究的目的:

为了研究铁 (Fe) 给药对大动脉铁过载和血管化 (VC) 的影响,在CKD的老鼠模型中.
为了确定Nrf2及其相关基因 (ferritin H,HIF-1α) 在Fe给药后VC的发展中的参与.

主要方法:

通过使用腺素和高Pi饮食,建立了一个CKD大鼠模型.
CKD大鼠接受了口服或腹腔内Fe的管理.
分析了大动脉中的Fe, (Ca) 和Pi含量,以及Nrf2,ferritin H,HIF-1α,HMOX1和NQO1mRNA水平.

主要成果:

腹腔内Fe的给药显著增加了大动脉Fe含量,与肝肝素 (HAMP) mRNA水平相关.
铁的使用并没有显著改变大动脉中的 (Ca) 或 (Pi) 含量.
大动脉Nrf2mRNA水平随着Fe的使用而增加,与大动脉Fe,血清Pi和ferritin H,HIF-1α,HMOX1和NQO1.1的mRNA水平相关.

结论:

亲肠道Fe给药会增加大动脉Fe和肝脏HAMPmRNA,但不会在CKD大鼠中加剧VC.
大动脉Nrf2mRNA水平与大动脉Fe和血清Pi显著相关,这表明它在氧化应激反应中发挥了作用.
Nrf2通路与费里H和HIF-1α一起,似乎参与了CKD中对Fe负载和氧化应激的反应.

关键词:

慢性脏疾病慢性脏疾病费里H 费里H 费里H 这就是HIF-1α.Nrf2 没有任何问题.是一种的物质.血管化是因为血管化.铁是铁,铁是铁,铁是铁.

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