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外源性核苷酸通过调节 AMPK 通路改善 SAMP8 小鼠心脏衰老

Exogenous Nucleotides Mitigate Cardiac Aging in SAMP8 Mice by Modulating Energy Metabolism Through AMPK Pathway.

机构信息

Department of Nutrition and Food Hygiene, School of Public Health, Peking University, Beijing 100191, China.

Beijing Key Laboratory of Toxicological Research and Risk Assessment for Food Safety, Peking University, Beijing 100191, China.

出版信息

Nutrients. 2024 Nov 11;16(22):3851. doi: 10.3390/nu16223851.

DOI:10.3390/nu16223851
PMID:39599637
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11597617/
Abstract

BACKGROUND

Cardiovascular disease (CVD) is the predominant cause of mortality, with aging being a significant risk factor. Nucleotides (NTs), essential for numerous biological functions, are particularly vital under conditions like aging, starvation, and nutrient deficiency. Although the antiaging benefits of exogenous NTs have been recognized in various systems, their cardiac-specific effects are not well understood. This study, therefore, investigated the impact of exogenous NTs on cardiac aging and delved into the potential mechanisms.

METHODS

Senescence-accelerated mouse prone-8 (SAMP8) mice were utilized, randomly assigned to one of three groups: a control group (Control), a low-dose NTs group (NTs_L), and a high-dose NTs group (NTs_H). Meanwhile, senescence-accelerated mouse resistant 1 (SAMR1) mice were set up as the SAMR1 group. Following a 9-month intervention, cardiac tissues were subjected to analysis.

RESULTS

The results showed that NTs improved the morphological structure of the cardiac tissue, enhanced the antioxidant capacity, and mitigated inflammation. Metabolomics analysis revealed that the high-dose NT intervention improved cardiac tissue energy metabolism, potentially through activating the AMPK pathway, enhanced mitochondrial biogenesis, and increased TFAM protein expression.

CONCLUSIONS

Together, these results indicate that exogenous NTs exert beneficial effects on the cardiac tissues of SAMP8 mice, potentially mitigating the cardiac aging process.

摘要

背景

心血管疾病（CVD）是主要的死亡原因，而衰老则是一个重要的风险因素。核苷酸（NTs）对于许多生物功能至关重要，特别是在衰老、饥饿和营养缺乏等情况下。尽管外源性 NTs 在各种系统中的抗衰老作用已得到认可，但它们在心脏方面的具体作用尚不清楚。因此，本研究探讨了外源性 NTs 对心脏衰老的影响，并深入研究了潜在的机制。

方法

使用衰老加速型小鼠易感 8 号（SAMP8）小鼠，随机分为三组：对照组（Control）、低剂量 NTs 组（NTs_L）和高剂量 NTs 组（NTs_H）。同时，设置衰老加速型小鼠抵抗 1 号（SAMR1）小鼠作为 SAMR1 组。经过 9 个月的干预后，对心脏组织进行分析。

结果

结果表明，NTs 改善了心脏组织的形态结构，增强了抗氧化能力，减轻了炎症。代谢组学分析显示，高剂量 NT 干预改善了心脏组织的能量代谢，可能通过激活 AMPK 途径、增强线粒体生物发生和增加 TFAM 蛋白表达来实现。

结论

综上所述，这些结果表明，外源性 NTs 对 SAMP8 小鼠的心脏组织具有有益作用，可能减缓心脏衰老过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/796cb566b0b1/nutrients-16-03851-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/527dd062cc4b/nutrients-16-03851-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/427b50825938/nutrients-16-03851-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/2479a0ecda4a/nutrients-16-03851-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/33dabc746e90/nutrients-16-03851-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/34a6aa8e2daf/nutrients-16-03851-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/5565a1c5dcc0/nutrients-16-03851-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/3fcce1f83f42/nutrients-16-03851-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/7362547657ec/nutrients-16-03851-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/b9cb980d972a/nutrients-16-03851-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/796cb566b0b1/nutrients-16-03851-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/527dd062cc4b/nutrients-16-03851-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/427b50825938/nutrients-16-03851-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/2479a0ecda4a/nutrients-16-03851-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/33dabc746e90/nutrients-16-03851-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/34a6aa8e2daf/nutrients-16-03851-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/5565a1c5dcc0/nutrients-16-03851-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/3fcce1f83f42/nutrients-16-03851-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/7362547657ec/nutrients-16-03851-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/b9cb980d972a/nutrients-16-03851-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ed6/11597617/796cb566b0b1/nutrients-16-03851-g010.jpg

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