补充 S-腺苷-L-蛋氨酸可减少炎症浸润,从而缓解主动脉夹层。

IF 3.9 2区 医学 Q2 NUTRITION & DIETETICS
Qian Wang, Jun An, Wei Zhou, Yujing Zhang, Jiang Huang, Geping Liao, Mingzhe Wang, Lingbo Xia, Aiping Le, Jianbing Zhu
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引用次数: 0

摘要

蛋氨酸是一种不可或缺的氨基酸,对膳食平衡至关重要,它错综复杂地控制着新陈代谢途径。破坏蛋氨酸的平衡有可能使血浆和组织中的同型半胱氨酸水平升高,从而有可能诱发炎症并损害血管内皮细胞的完整性。甲硫氨酸代谢(特别是 S-腺苷-L-甲硫氨酸(SAM))与胸主动脉夹层(TAD)的发病之间错综复杂的相互作用仍是一个谜,尽管人们承认炎症在这种血管疾病中起着关键作用。在一个由β-氨基丙腈单富马酸盐(BAPN)诱导的小鼠模型中,我们深入研究了补充S-腺苷-L-蛋氨酸(SAM)对TAD进展的影响。我们的观察发现,补充 SAM 后,主动脉夹层和破裂率明显改善,死亡率显著降低。值得注意的是,补充 SAM 对 BAPN 诱导的弹性蛋白和细胞外基质降解具有相当大的保护作用。此外,补充 SAM 对免疫细胞,尤其是中性粒细胞和巨噬细胞的浸润有很强的抑制作用。它还显著降低了巨噬细胞的炎症极化,表现在巨噬细胞中 MHC-II 高的巨噬细胞聚集减少,以及 IL1β 和 TNFα 等炎症细胞因子的表达减少。同时,补充 SAM 还能抑制主动脉中 CD4 + 和 CD8 + T 细胞的活化。这表现为 CD44- CD62L + 天真 T 细胞比例升高,CD44 + CD62L- 效应 T 细胞同时减少。总之,我们的研究结果有力地表明,补充 SAM 在缓解 BAPN 诱导的主动脉炎症方面具有显著疗效,从而阻碍了胸主动脉夹层的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
S-adenosyl-L-methionine supplementation alleviates aortic dissection by decreasing inflammatory infiltration.

Methionine, an indispensable amino acid crucial for dietary balance, intricately governs metabolic pathways. Disruption in its equilibrium has the potential to heighten homocysteine levels in both plasma and tissues, posing a conceivable risk of inducing inflammation and detriment to the integrity of vascular endothelial cells. The intricate interplay between methionine metabolism, with a specific focus on S-adenosyl-L-methionine (SAM), and the onset of thoracic aortic dissection (TAD) remains enigmatic despite acknowledging the pivotal role of inflammation in this vascular condition. In an established murine model induced by β-aminopropionitrile monofumarate (BAPN), we delved into the repercussions of supplementing with S-adenosyl-L-methionine (SAM) on the progression of TAD. Our observations uncovered a noteworthy improvement in aortic dissection and rupture rates, accompanied by a marked reduction in mortality upon SAM supplementation. Notably, SAM supplementation exhibited a considerable protective effect against BAPN-induced degradation of elastin and the extracellular matrix. Furthermore, SAM supplementation demonstrated a robust inhibitory influence on the infiltration of immune cells, particularly neutrophils and macrophages. It also manifested a notable reduction in the inflammatory polarization of macrophages, evident through diminished accumulation of MHC-IIhigh macrophages and reduced expression of inflammatory cytokines such as IL1β and TNFα in macrophages. Simultaneously, SAM supplementation exerted a suppressive effect on the activation of CD4 + and CD8 + T cells within the aorta. This was evidenced by an elevated proportion of CD44- CD62L + naïve T cells and a concurrent decrease in CD44 + CD62L- effector T cells. In summary, our findings strongly suggest that the supplementation of SAM exhibits remarkable efficacy in alleviating BAPN-induced aortic inflammation, consequently impeding the progression of thoracic aortic dissection.

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来源期刊
Nutrition & Metabolism
Nutrition & Metabolism 医学-营养学
CiteScore
8.40
自引率
0.00%
发文量
78
审稿时长
4-8 weeks
期刊介绍: Nutrition & Metabolism publishes studies with a clear focus on nutrition and metabolism with applications ranging from nutrition needs, exercise physiology, clinical and population studies, as well as the underlying mechanisms in these aspects. The areas of interest for Nutrition & Metabolism encompass studies in molecular nutrition in the context of obesity, diabetes, lipedemias, metabolic syndrome and exercise physiology. Manuscripts related to molecular, cellular and human metabolism, nutrient sensing and nutrient–gene interactions are also in interest, as are submissions that have employed new and innovative strategies like metabolomics/lipidomics or other omic-based biomarkers to predict nutritional status and metabolic diseases. Key areas we wish to encourage submissions from include: -how diet and specific nutrients interact with genes, proteins or metabolites to influence metabolic phenotypes and disease outcomes; -the role of epigenetic factors and the microbiome in the pathogenesis of metabolic diseases and their influence on metabolic responses to diet and food components; -how diet and other environmental factors affect epigenetics and microbiota; the extent to which genetic and nongenetic factors modify personal metabolic responses to diet and food compositions and the mechanisms involved; -how specific biologic networks and nutrient sensing mechanisms attribute to metabolic variability.
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