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L-精氨酸通过维持细胞外基质和降低淋巴细胞的细胞毒性活性来改善实验性自身免疫性心肌炎。

L-arginine ameliorates experimental autoimmune myocarditis by maintaining extracellular matrix and reducing cytotoxic activity of lymphocytes.

作者信息

Okabe Taka-aki, Hattori Miki, Yuan Zuyi, Kishimoto Chiharu

机构信息

Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

出版信息

Int J Exp Pathol. 2008 Oct;89(5):382-8. doi: 10.1111/j.1365-2613.2008.00609.x.

DOI:10.1111/j.1365-2613.2008.00609.x
PMID:18808530
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2613980/
Abstract

It was previously shown that administration of the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) aggravated murine viral myocarditis by increasing myocardial virus titres. Experimental autoimmune myocarditis in mice and rats mimics human fulminant myocarditis. The effects of L-arginine, a precursor of nitric oxide, upon heart failure in experimental autoimmune myocarditis were evaluated. Dietary L-arginine (L-arginine group) and L-arginine plus N(G)-nitro-L-arginine methyl ester (L-arginine + l-NAME group) were administered to C57BL/6 mice immunized with porcine cardiac myosin over 3 weeks. An untreated myocarditis group was prepared. Cardiac damage was less in the L-arginine group compared with the other two groups, as was incidence of heart failure. In addition, extracellular matrix change was less prominent in the L-arginine group. Plasma concentrations of nitric oxide were elevated in the L-arginine group. Cytotoxic activities of lymphocytes were lower in L-arginine group than in other two groups. L-arginine treatment may be effective in preventing the development of heart failure in experimental myocarditis by maintaining extracellular matrix and reducing the cytotoxic activity of lymphocytes.

摘要

先前的研究表明,给予一氧化氮合酶抑制剂N(G)-硝基-L-精氨酸甲酯(L-NAME)会通过增加心肌病毒滴度而加重小鼠病毒性心肌炎。小鼠和大鼠的实验性自身免疫性心肌炎模拟人类暴发性心肌炎。评估了一氧化氮的前体L-精氨酸对实验性自身免疫性心肌炎心力衰竭的影响。在3周内,将饮食中的L-精氨酸(L-精氨酸组)和L-精氨酸加N(G)-硝基-L-精氨酸甲酯(L-精氨酸+L-NAME组)给予用猪心肌肌凝蛋白免疫的C57BL/6小鼠。制备未治疗的心肌炎组。与其他两组相比,L-精氨酸组的心脏损伤较轻,心力衰竭的发生率也较低。此外,L-精氨酸组的细胞外基质变化不那么明显。L-精氨酸组的血浆一氧化氮浓度升高。L-精氨酸组淋巴细胞的细胞毒性活性低于其他两组。L-精氨酸治疗可能通过维持细胞外基质和降低淋巴细胞的细胞毒性活性,有效预防实验性心肌炎中心力衰竭的发展。

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Foxp3 controls regulatory T-cell function by interacting with AML1/Runx1.Foxp3通过与AML1/Runx1相互作用来控制调节性T细胞的功能。
Nature. 2007 Apr 5;446(7136):685-9. doi: 10.1038/nature05673. Epub 2007 Mar 21.
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Cationic amino acid transporter 2 regulates inflammatory homeostasis in the lung.阳离子氨基酸转运体2调节肺部的炎症稳态。
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Foxp3+ CD25+ CD4+ natural regulatory T cells in dominant self-tolerance and autoimmune disease.Foxp3 + CD25 + CD4 + 自然调节性T细胞在显性自身耐受和自身免疫性疾病中的作用
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