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表没食子儿茶素没食子酸酯（EGCG）通过整合代谢组学和网络药理学在肥胖相关性早熟中的治疗作用及潜在机制。

The therapeutic role and potential mechanism of EGCG in obesity-related precocious puberty as determined by integrated metabolomics and network pharmacology.

机构信息

Department of Nutrition, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Department of Nutrition, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

出版信息

Front Endocrinol (Lausanne). 2023 Jun 2;14:1159657. doi: 10.3389/fendo.2023.1159657. eCollection 2023.

DOI:10.3389/fendo.2023.1159657
PMID:37334310
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10272822/
Abstract

OBJECTIVE

(-)-Epigallocatechin-3-gallate (EGCG) has preventive effects on obesity-related precocious puberty, but its underlying mechanism remains unclear. The aim of this study was to integrate metabolomics and network pharmacology to reveal the mechanism of EGCG in the prevention of obesity-related precocious puberty.

MATERIALS AND METHODS

A high-performance liquid chromatography-electrospray ionization ion-trap tandem mass spectrometry (LC-ESI-MS/MS) was used to analyze the impact of EGCG on serum metabolomics and associated metabolic pathways in a randomized controlled trial. Twelve weeks of EGCG capsules were given to obese girls in this trail. Additionally, the targets and pathways of EGCG in preventing obesity-related precocious puberty network pharmacology were predicted using network pharmacology. Finally, the mechanism of EGCG prevention of obesity-related precocious puberty was elucidated through integrated metabolomics and network pharmacology.

RESULTS

Serum metabolomics screened 234 endogenous differential metabolites, and network pharmacology identified a total of 153 common targets. These metabolites and targets mainly enrichment pathways involving endocrine-related pathways (estrogen signaling pathway, insulin resistance, and insulin secretion), and signal transduction (PI3K-Akt, MAPK, and Jak-STAT signaling pathways). The integrated metabolomics and network pharmacology indicated that AKT1, EGFR, ESR1, STAT3, IGF1, and MAPK1 may be key targets for EGCG in preventing obesity-related precocious puberty.

CONCLUSION

EGCG may contribute to preventing obesity-related precocious puberty through targets such as AKT1, EGFR, ESR1, STAT3, IGF1, and MAPK1 and multiple signaling pathways, including the estrogen, PI3K-Akt, MAPK, and Jak-STAT pathways. This study provided a theoretical foundation for future research.

摘要

目的

（-）-表没食子儿茶素没食子酸酯（EGCG）对肥胖相关性性早熟具有预防作用，但作用机制尚不清楚。本研究旨在整合代谢组学和网络药理学，揭示 EGCG 预防肥胖相关性性早熟的作用机制。

材料与方法

采用高效液相色谱-电喷雾离子阱串联质谱（LC-ESI-MS/MS）分析 EGCG 对肥胖女孩血清代谢组学及相关代谢途径的影响。在这项试验中，肥胖女孩连续 12 周服用 EGCG 胶囊。此外，采用网络药理学预测 EGCG 预防肥胖相关性性早熟的靶点和途径。最后，通过整合代谢组学和网络药理学探讨 EGCG 预防肥胖相关性性早熟的作用机制。

结果

血清代谢组学筛选出 234 个内源性差异代谢物，网络药理学共预测到 153 个共同靶点。这些代谢物和靶点主要富集在内分泌相关途径（雌激素信号通路、胰岛素抵抗和胰岛素分泌）和信号转导（PI3K-Akt、MAPK 和 Jak-STAT 信号通路）。整合代谢组学和网络药理学表明，AKT1、EGFR、ESR1、STAT3、IGF1 和 MAPK1 可能是 EGCG 预防肥胖相关性性早熟的关键靶点。

结论

EGCG 可能通过 AKT1、EGFR、ESR1、STAT3、IGF1 和 MAPK1 等靶点以及雌激素、PI3K-Akt、MAPK 和 Jak-STAT 等多种信号通路发挥预防肥胖相关性性早熟的作用。本研究为进一步研究提供了理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/891c/10272822/5bb086a5066e/fendo-14-1159657-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/891c/10272822/32d6b428df5d/fendo-14-1159657-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/891c/10272822/74f3b7a83678/fendo-14-1159657-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/891c/10272822/79f3d3a42024/fendo-14-1159657-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/891c/10272822/ce4ada89f319/fendo-14-1159657-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/891c/10272822/7cda811a5573/fendo-14-1159657-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/891c/10272822/5bb086a5066e/fendo-14-1159657-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/891c/10272822/32d6b428df5d/fendo-14-1159657-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/891c/10272822/74f3b7a83678/fendo-14-1159657-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/891c/10272822/79f3d3a42024/fendo-14-1159657-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/891c/10272822/ce4ada89f319/fendo-14-1159657-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/891c/10272822/7cda811a5573/fendo-14-1159657-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/891c/10272822/5bb086a5066e/fendo-14-1159657-g006.jpg

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