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整合代谢组学与网络药理学以探究人参皂苷Re对小鼠放疗损伤的保护作用

Integrating Metabolomics and Network Pharmacology to Explore the Protective Effect of Ginsenoside Re against Radiotherapy Injury in Mice.

作者信息

Yu Chunmiao, Fu Jiaqi, Guo Lidong, Yu Miaomiao, Yu Donghua

机构信息

Heilongjiang University of Chinese Medicine, Harbin 150040, China.

出版信息

Evid Based Complement Alternat Med. 2022 Mar 11;2022:5436979. doi: 10.1155/2022/5436979. eCollection 2022.

DOI:10.1155/2022/5436979
PMID:35310032
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8933113/
Abstract

Ionizing radiation (IR) can cause radiation damage, mutagenesis, or carcinogenesis in the irradiated subject. It is manifested as metabolic disorders of the body and damage to the immune system, nervous system, and endocrine system, which can lead to physiological and pathological changes and endogenous metabolic disorders. Ginsenoside Re (G-Re), a single component of traditional Chinese medicine, has a certain ameliorating effect on radiation damage. However, its mechanism of action in the treatment of radiotherapy injury remains unclear. With this purpose, the hematopoietic function of mice damaged by X-ray radiation was studied, and the protective effect of G-Re on mice damaged by radiation was preliminarily evaluated. Network pharmacology and metabolomics analysis are used to further reveal the mechanism of G-Re to improve radiation damage through metabolomics research. Results of metabolomics analysis showed that 16 potential biomarkers were identified as participating in the therapeutic effect of G-Re on IR. Most of these metabolites are adjusted to recover after G-Re treatment. The pathways involved included glycerophospholipid metabolism, sphingolipid metabolism, and linoleic acid metabolism. According to network pharmacology analysis, we found 10 hub genes, which is partly consistent with the findings of metabolomics. Further comprehensive analysis focused on 4 key targets, including SRC, EGFR, AKT1, and MAPK8, and their related core metabolites and pathways. This study combines metabolomics and network pharmacology analysis to explore the key targets and mechanisms of G-Re in the treatment of IR, in order to provide new strategies for clinical treatment of radiotherapy injury.

摘要

电离辐射(IR)可导致受照对象出现辐射损伤、诱变或致癌。其表现为机体代谢紊乱以及免疫系统、神经系统和内分泌系统受损,进而可引发生理和病理变化以及内源性代谢紊乱。人参皂苷Re(G-Re)是一种中药单体成分,对辐射损伤具有一定的改善作用。然而,其治疗放疗损伤的作用机制尚不清楚。基于此目的,研究了X射线辐射损伤小鼠的造血功能,并初步评估了G-Re对辐射损伤小鼠的保护作用。通过代谢组学研究,利用网络药理学和代谢组学分析进一步揭示G-Re改善辐射损伤的机制。代谢组学分析结果显示,鉴定出16种潜在生物标志物参与G-Re对IR的治疗作用。这些代谢物中的大多数在G-Re治疗后得到调整恢复。涉及的途径包括甘油磷脂代谢、鞘脂代谢和亚油酸代谢。根据网络药理学分析,我们发现了10个核心基因,这与代谢组学的研究结果部分一致。进一步的综合分析聚焦于4个关键靶点,包括SRC、EGFR、AKT1和MAPK8,以及它们相关的核心代谢物和途径。本研究结合代谢组学和网络药理学分析,探索G-Re治疗IR的关键靶点和机制,以期为放疗损伤的临床治疗提供新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/619c/8933113/36e2465d9afd/ECAM2022-5436979.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/619c/8933113/e43a2db18864/ECAM2022-5436979.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/619c/8933113/514037467fae/ECAM2022-5436979.002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/619c/8933113/338fcf968a5e/ECAM2022-5436979.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/619c/8933113/36e2465d9afd/ECAM2022-5436979.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/619c/8933113/e43a2db18864/ECAM2022-5436979.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/619c/8933113/514037467fae/ECAM2022-5436979.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/619c/8933113/c5d8ad8c5436/ECAM2022-5436979.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/619c/8933113/338fcf968a5e/ECAM2022-5436979.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/619c/8933113/36e2465d9afd/ECAM2022-5436979.005.jpg

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