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人参皂苷Rh2及其辛酯衍生物在癌症治疗中抗血管生成的分子机制：PI3K和ROS之间的斗争

IF 6.8 2区医学 Q1 CHEMISTRY, MEDICINAL

Journal of Ginseng Research Pub Date : 2025-01-11 DOI:10.1016/j.jgr.2025.01.002

Qi-Rui Hu , Xin-Yi Zhong , Hua Feng , Xu-Chu Li , Zhi-Hong Zhang , Yao Pan , Ting Luo , Ze-Yuan Deng , Fang Chen

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引用次数: 0

摘要

背景以血管内皮生长因子A （VEGFA）诱导的肿瘤相关血管生成（TAA）为靶点的肿瘤治疗越来越受到重视。人参皂苷Rh2已被证明通过VEGFA抑制TAA。然而，潜在的机制仍不清楚。此外，在我们前期的研究中，Rh2的辛酯衍生物（Rh2- o）对肝癌的抑制作用优于Rh2，这表明Rh2- o也可能对TAA有抑制作用。目的探讨Rh2和Rh2- o对TAA的抑制作用及其机制。方法通过条件培养基、共培养和荷瘤小鼠实验，评价Rh2和Rh2- o对TAA的抑制作用。网络药理学用于探索可能的靶点，随后由特异性激动剂或抑制剂验证。结果rh2和Rh2-O能有效抑制TAA，且呈剂量依赖性(P <；0.05)。此外，增强PI3K和STAT3的磷酸化可以逆转Rh2和Rh2- o对TAA的抑制作用，而n -乙酰半胱氨酸可以改善这种抑制作用(P <；0.05)。结论rh2和Rh2-O通过PI3K/STAT3和PI3K/HIF-1α途径抑制VEGFA抑制TAA。同时，ROS的生成可能是Rh2和Rh2- o抑制TAA的敌人。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

The molecular mechanism of ginsenoside Rh2 and its octyl ester derivative on anti-angiogenesis in cancer treatment: The battle between PI3K and ROS

查看原文本刊更多论文

The molecular mechanism of ginsenoside Rh2 and its octyl ester derivative on anti-angiogenesis in cancer treatment: The battle between PI3K and ROS

Background

The cancer treatments that target tumor associated angiogenesis (TAA) induced by vascular endothelial growth factor A (VEGFA) have become valued. Ginsenoside Rh2 has been proved to inhibit TAA through VEGFA. However, the underlying mechanisms remain unclear. Moreover, the octyl ester derivative of Rh2 (Rh2-O) exhibited better inhibitory effects than Rh2 on liver cancer in our previous researches, which indicated that Rh2-O might also exert inhibitory effects on TAA.

Purpose

To explore the inhibitory effects of Rh2 and Rh2-O on TAA and to investigate the underlying mechanisms.

Method

The inhibitory effects of Rh2 and Rh2-O on TAA were evaluated by conditioned medium, co-culture, and tumor-bearing mice. The network pharmacology was used to explore the possible targets, which were subsequently verified by specific agonists or inhibitors.

Results

Rh2 and Rh2-O could efficiently inhibit TAA in a dose-dependent manner (P < 0.05). Moreover, the enhancement on phosphorylation of PI3K and STAT3 could reverse the inhibitory effects of Rh2 and Rh2-O on TAA while N-acetylcysteine could improve the effects (P < 0.05).

Conclusion

Rh2 and Rh2-O could inhibit TAA via inhibiting the VEGFA, which was mediated by PI3K/STAT3 and PI3K/HIF-1α pathway. Meanwhile the generation of ROS could be a foe for Rh2 and Rh2-O to inhibit TAA.

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来源期刊

Journal of Ginseng Research

Journal of Ginseng Research CHEMISTRY, MEDICINAL-INTEGRATIVE & COMPLEMENTARY MEDICINE

CiteScore

11.40

自引率

9.50%

发文量

111

审稿时长

6-12 weeks

期刊介绍： Journal of Ginseng Research (JGR) is an official, open access journal of the Korean Society of Ginseng and is the only international journal publishing scholarly reports on ginseng research in the world. The journal is a bimonthly peer-reviewed publication featuring high-quality studies related to basic, pre-clinical, and clinical researches on ginseng to reflect recent progresses in ginseng research. JGR publishes papers, either experimental or theoretical, that advance our understanding of ginseng science, including plant sciences, biology, chemistry, pharmacology, toxicology, pharmacokinetics, veterinary medicine, biochemistry, manufacture, and clinical study of ginseng since 1976. It also includes the new paradigm of integrative research, covering alternative medicinal approaches. Article types considered for publication include review articles, original research articles, and brief reports. JGR helps researchers to understand mechanisms for traditional efficacy of ginseng and to put their clinical evidence together. It provides balanced information on basic science and clinical applications to researchers, manufacturers, practitioners, teachers, scholars, and medical doctors.

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