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硒对异丙肾上腺素诱导的实验性大鼠心肌梗死后白三烯 B4 合成途径的影响。

Impact of selenium on the leukotriene B4 synthesis pathway during isoproterenol-induced myocardial infarction in experimental rats.

机构信息

Department of Biochemistry, University of Kerala, Kariavattom Campus, 695581, Thiruvananthapuram, India.

出版信息

Inflammation. 2012 Feb;35(1):74-80. doi: 10.1007/s10753-010-9291-3.

DOI:10.1007/s10753-010-9291-3
PMID:21274744
Abstract

Selenium (Se), an essential micronutrient, exerts its biological functions through selenoproteins. There are evidences that show Se to have an impact on the course and outcome of a number of etiologically inflammatory diseases. Leukotriene B(4) (LTB(4)) is an inflammatory mediator, and its production is mediated through two specific enzymes--lipooxygenase (LOX) and leukotriene A(4) hydrolase (LTA(4)H). We examined the effect of Se on LTB(4) synthesis during isoproterenol (ISP)-induced myocardial infarction (MI) in rats. Rats were divided as: control, ISP, Se, and Se + ISP. Sodium selenite was administered at dose of 8 μg/100 g/day. ISP was injected subcutaneously twice (10 mg/100 g body weight). The rats pretreated with Se had increased concentration of phospholipids and enhanced biosynthetic enzymes compared with that of ISP. The activities of phospholipases decreased on Se treatment. The level of calcium was increased in ISP group whereas, on Se treatment, it was near normal levels. Activities of LOX and expression of LTA(4)H were down-regulated in the case of Se-pretreated rats. Our study shows the anti-inflammatory mechanism of selenium during MI.

摘要

硒(Se)是一种必需的微量元素,通过硒蛋白发挥其生物学功能。有证据表明,硒对许多病因学上的炎症性疾病的过程和结果有影响。白三烯 B4(LTB4)是一种炎症介质,其产生通过两种特定的酶——脂氧合酶(LOX)和白三烯 A4 水解酶(LTA4H)来介导。我们研究了硒对异丙肾上腺素(ISP)诱导的大鼠心肌梗死(MI)期间 LTB4 合成的影响。大鼠分为:对照组、ISP 组、硒组和硒+ISP 组。亚硒酸钠的给药剂量为 8μg/100g/天。ISP 皮下注射两次(10mg/100g 体重)。与 ISP 组相比,用硒预处理的大鼠的磷脂浓度增加,生物合成酶增强。用硒处理后,磷脂酶的活性降低。ISP 组的钙水平升高,而在用硒处理后,钙水平接近正常水平。LOX 的活性和 LTA4H 的表达在硒预处理的大鼠中下调。我们的研究表明,硒在 MI 期间具有抗炎机制。

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本文引用的文献

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Eicosanoid signalling pathways in the heart.心脏中的类花生酸信号通路。
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细胞内钙和磷脂酶A2在过表达CYP2E1的肝细胞中花生四烯酸诱导的毒性中的作用。
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