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人参皂苷Rg3通过代谢产物组蛋白H3在肺癌中发挥抗癌作用。

Ginsenoside Rg3 exerts anticancer effects in lung cancer through metabolite Histon H3.

作者信息

Xiao Huiyan, Zhang Yongcong, Zhang Banghui, Wu Jian, Li Xu

机构信息

Department of Clean Operating, Quanzhou First Hospital Quanzhou 362002, Fujian, China.

Department of Thoracic Surgery, Quanzhou First Hospital Quanzhou 362002, Fujian, China.

出版信息

Am J Transl Res. 2025 May 15;17(5):3994-4007. doi: 10.62347/YJZW4664. eCollection 2025.

Abstract

OBJECTIVES

To investigate the effects of ginsenoside Rg3 on metabolites in lung cancer cells.

METHODS

A549 cells were inoculated into nude BALB/c mice. Ginsenoside Rg3 (0.2 mL) or normal saline was orally administered daily for 12 days. LC/MS-based metabolomics was performed to analyze the metabolite profiles across three groups.

RESULTS

In serum samples, 143 metabolites were significantly different between the model and ginsenoside Rg3 groups. In fecal samples, 44 metabolites differed significantly between the two groups. Levels of Lamin A/C and Histon H3 were upregulated in model tissues. Ginsenoside Rg3 treatment significantly inhibited the expression of Lamin A/C and Histon H3, suggesting inhibition of histidine metabolism activation in lung cancer. Furthermore, ginsenoside Rg3 or Lamin A knockdown inhibited histamine-induced proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in lung cancer cells.

CONCLUSIONS

Ginsenoside Rg3 significantly altered the metabolic profile in lung cancer mice. Mechanistically, ginsenoside Rg3 downregulated Lamin A/C through histidine metabolic pathway and suppressed histamine-induced progression of lung cancer.

摘要

目的

研究人参皂苷Rg3对肺癌细胞代谢产物的影响。

方法

将A549细胞接种到BALB/c裸鼠体内。每天口服给予人参皂苷Rg3(0.2 mL)或生理盐水,持续12天。采用基于液相色谱/质谱联用的代谢组学技术分析三组的代谢产物谱。

结果

在血清样本中,模型组与人参皂苷Rg3组之间有143种代谢产物存在显著差异。在粪便样本中,两组之间有44种代谢产物存在显著差异。模型组织中核纤层蛋白A/C和组蛋白H3水平上调。人参皂苷Rg3处理显著抑制了核纤层蛋白A/C和组蛋白H3的表达,提示其对肺癌中组氨酸代谢激活的抑制作用。此外,人参皂苷Rg3或核纤层蛋白A基因敲低可抑制组胺诱导的肺癌细胞增殖、迁移、侵袭及上皮-间质转化(EMT)。

结论

人参皂苷Rg3显著改变了肺癌小鼠的代谢谱。机制上,人参皂苷Rg3通过组氨酸代谢途径下调核纤层蛋白A/C,并抑制组胺诱导的肺癌进展。

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