摄入精氨酸可抑制大鼠快肌收缩时吞噬细胞的入侵

IF 1.8 3区 生物学 Q4 CELL BIOLOGY
Keita Kanzaki, Masanobu Wada
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引用次数: 0

摘要

研究表明,偏心收缩(ECC)可诱导白细胞侵入骨骼肌,从而导致肌肉炎症。本研究旨在探讨事先摄入一氧化氮前体--L-精氨酸(ARG)是否能抑制 ECC 诱导的巨噬细胞入侵。雄性 Wistar 大鼠在 ECC 前 3 天开始连续 7 天在水中摄入 ARG。在胸骨前肌诱导 ECC 200 次。三天后,切除胫骨前肌和趾长伸肌,分别进行生化分析和力量测量。摄入 ARG 可提高血浆和肌肉中的亚硝酸盐和硝酸盐水平,抑制 ECC 肌肉的力量抑制并降低 CD68 含量。摄入 ARG 还能改善 ECC 诱导的蛋白质硝化增加,但摄入 ARG 和 ECC 诱导都不会影响蛋白质的羰基水平。本研究结果表明,摄入 ARG 或富含 ARG 的食物可通过减轻吞噬细胞对偏心收缩骨骼肌的侵袭来缓解炎症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Arginine ingestion inhibits phagocyte invasion in eccentrically contracted rat fast-twitch muscle

Arginine ingestion inhibits phagocyte invasion in eccentrically contracted rat fast-twitch muscle

Eccentric contraction (ECC) has been shown to induce leukocyte invasion into skeletal muscle, resulting in muscle inflammation. This study aimed to investigate whether prior ingestion of L-arginine (ARG), a nitric oxide precursor, inhibits ECC-induced macrophage invasion. Male Wistar rats received ARG in water for 7 days, beginning 3 days prior to ECC. ECCs were induced in the anterior crural muscles for 200 cycles. Three days later, the tibialis anterior and extensor digitorum longus muscles were excised for biochemical analysis and force measurement, respectively. ARG ingestion increased nitrite and nitrate levels in plasma and muscle, inhibiting force depression and reducing CD68 content in muscles subjected to ECC. ARG ingestion also ameliorated an ECC-induced increase in protein nitration, although neither ARG ingestion nor ECC induction affected protein carbonyl levels. The present results suggest that ingestion of ARG or ARG-rich foods may alleviate inflammation by attenuating phagocyte invasion in eccentrically contracted skeletal muscles.

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来源期刊
CiteScore
6.20
自引率
0.00%
发文量
21
审稿时长
>12 weeks
期刊介绍: The Journal of Muscle Research and Cell Motility has as its main aim the publication of original research which bears on either the excitation and contraction of muscle, the analysis of any one of the processes involved therein, the processes underlying contractility and motility of animal and plant cells, the toxicology and pharmacology related to contractility, or the formation, dynamics and turnover of contractile structures in muscle and non-muscle cells. Studies describing the impact of pathogenic mutations in genes encoding components of contractile structures in humans or animals are welcome, provided they offer mechanistic insight into the disease process or the underlying gene function. The policy of the Journal is to encourage any form of novel practical study whatever its specialist interest, as long as it falls within this broad field. Theoretical essays are welcome provided that they are concise and suggest practical ways in which they may be tested. Manuscripts reporting new mutations in known disease genes without validation and mechanistic insight will not be considered. It is the policy of the journal that cells lines, hybridomas and DNA clones should be made available by the developers to any qualified investigator. Submission of a manuscript for publication constitutes an agreement of the authors to abide by this principle.
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