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.
Highlights
Ionizing radiation (IR) refers to the general term for radiation that can cause ionization of affecting substances, including X-rays, charged particles of α and β, and uncharged neutrons
By matching potential targets identified in network pharmacology with genes in MetScape analysis, we found GSR and PLA2G2 are related to oxidized glutathione and linoleic acid, and PPP5, ROCK1, ROCK2, AKT1, AKT2, CDK2, MAPK8, Epidermal growth factor receptor (EGFR), IGF1R, CSF1R, NTRK2, NTRK1, SRC, and SYK are related to palmitic acid, dodecanoic acid, and myristic acid (Table 6). ey may play an important role in the therapeutic effect of Ginsenoside Re (G-Re) on IR
We found that compared with the normal group, the content of phosphatidylcholine in the radiation model group was reduced, and the decrease in PC content after ionizing radiation may be due to radiation-induced damage to body cells and accelerated metabolism, thereby increasing the absorption of PC in the blood, while the content of the G-Re group was significant upregulation, which may inhibit cell damage caused by IR and protect cell integrity by unregulated phosphatidylcholine
Summary
Ionizing radiation (IR) refers to the general term for radiation that can cause ionization of affecting substances, including X-rays, charged particles of α and β, and uncharged neutrons It has the characteristics of high energy, high frequency, and short wavelength [1]. Radiation injury is a pathological state caused by ionizing radiation, which can result in a series of changes in metabolites Many of these studies are based on the search for biomarkers related to radiation dose in metabolites that can be used for early diagnosis and early warning of radiation damage. G-Re is considered to be an auxiliary drug for exogenous radiotherapy to study its radiation protection effect on organisms and its mechanism
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