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非靶向和靶向代谢组学相结合揭示人参须根延缓衰老的机制

Combined non-targeted and targeted metabolomics reveals the mechanism of delaying aging of Ginseng fibrous root.

作者信息

Yang Xiang, Yang Xiang, Li Bo, Zhang Jianyun, Yan Zhuyun

机构信息

State Key Laboratory of Characteristic Chinese Medicine Resources in Southwest China, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China.

Shijiazhuang Food and Drug Inspection Center, Shijiazhuang, China.

出版信息

Front Pharmacol. 2024 Jul 24;15:1368776. doi: 10.3389/fphar.2024.1368776. eCollection 2024.

DOI:10.3389/fphar.2024.1368776
PMID:39114359
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11303238/
Abstract

The fibrous root of ginseng (GFR) is the dried thin branch root or whisker root of Ginseng ( C. A. Mey). It is known for its properties such as tonifying qi, producing body fluid, and quenching thirst. Clinically, it is used to treat conditions such as cough, hemoptysis, thirst, stomach deficiency, and vomiting. While GFR and Ginseng share similar metabolites, they differ in their metabolites ratios and efficacy. Furthermore, the specific role of GFR in protecting the body remains unclear. We employed ultra-high performance liquid chromatography-triple quadrupole mass spectrometry to examine alterations in brain neurotransmitters and elucidate the impact of GFR on the central nervous system. Additionally, we analyzed the serum and brain metabolic profiles of rats using ultra-high performance liquid chromatography-quadrupole-orbitrap mass spectrometry to discern the effect and underlying mechanism of GFR in delaying aging in naturally aged rats. The findings of the serum biochemical indicators indicate that the intervention of GFR can enhance cardiovascular, oxidative stress, and energy metabolism related indicators in naturally aging rats. Research on brain neurotransmitters suggests that GFR can augment physiological functions such as learning and memory, while also inhibiting central nervous system excitation to a certain degree by maintaining the equilibrium of central neurotransmitters in aged individuals. Twenty-four abnormal metabolites in serum and seventeen abnormal metabolites in brain could be used as potential biomarkers and were involved in multiple metabolic pathways. Among them, in the brain metabolic pathways, alanine, aspartate and glutamate metabolism, arginine and proline metabolism, histidine metabolism, and tyrosine metabolism were closely related to central neurotransmitters. Butanoate metabolism improves energy supply for life activities in the aging body. Cysteine and methionine metabolism contributes to the production of glutathione and taurine and played an antioxidant role. In serum, the regulation of glycerophospholipid metabolism pathway and proline metabolism demonstrated the antioxidant capacity of GFR decoction. In summary, GFR plays a role in delaying aging by regulating central neurotransmitters, cardiovascular function, oxidative stress, energy metabolism, and other aspects of the aging body, which lays a foundation for the application of GFR.

摘要

人参须根(GFR)是人参(C. A. Mey)干燥的细支根或须根。它以补气、生津、止渴等功效著称。临床上,它用于治疗咳嗽、咯血、口渴、胃虚和呕吐等病症。虽然人参须根与人参有相似的代谢产物,但它们在代谢产物比例和功效上有所不同。此外,人参须根在保护身体方面的具体作用仍不清楚。我们采用超高效液相色谱 - 三重四极杆质谱法检测脑内神经递质的变化,以阐明人参须根对中枢神经系统的影响。此外,我们使用超高效液相色谱 - 四极杆 - 轨道阱质谱法分析大鼠的血清和脑代谢谱,以识别人参须根在延缓自然衰老大鼠衰老过程中的作用及潜在机制。血清生化指标的研究结果表明,人参须根的干预可增强自然衰老大鼠心血管、氧化应激和能量代谢相关指标。对脑内神经递质的研究表明,人参须根可增强学习和记忆等生理功能,同时通过维持老年个体中枢神经递质的平衡,在一定程度上抑制中枢神经系统兴奋。血清中的24种异常代谢产物和脑内的17种异常代谢产物可作为潜在生物标志物,并参与多种代谢途径。其中,在脑代谢途径中,丙氨酸、天冬氨酸和谷氨酸代谢、精氨酸和脯氨酸代谢、组氨酸代谢以及酪氨酸代谢与中枢神经递质密切相关。丁酸代谢改善衰老机体生命活动的能量供应。半胱氨酸和甲硫氨酸代谢有助于谷胱甘肽和牛磺酸的产生,并发挥抗氧化作用。在血清中,甘油磷脂代谢途径和脯氨酸代谢的调节表明人参须根水煎液具有抗氧化能力。综上所述,人参须根通过调节中枢神经递质、心血管功能、氧化应激、能量代谢等衰老机体的多个方面发挥延缓衰老的作用,为人参须根的应用奠定了基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/c01d1edc27d3/fphar-15-1368776-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/11b2c34d021e/fphar-15-1368776-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/2b20bab2908f/fphar-15-1368776-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/b38143b5e6a9/fphar-15-1368776-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/b0100d746813/fphar-15-1368776-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/24985237b314/fphar-15-1368776-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/265cf472f644/fphar-15-1368776-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/6841c566e058/fphar-15-1368776-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/d01d5967c168/fphar-15-1368776-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/c01d1edc27d3/fphar-15-1368776-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/11b2c34d021e/fphar-15-1368776-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/2b20bab2908f/fphar-15-1368776-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/b38143b5e6a9/fphar-15-1368776-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/b0100d746813/fphar-15-1368776-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/24985237b314/fphar-15-1368776-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/265cf472f644/fphar-15-1368776-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/6841c566e058/fphar-15-1368776-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/d01d5967c168/fphar-15-1368776-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63a3/11303238/c01d1edc27d3/fphar-15-1368776-g009.jpg

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