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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2025.3
- 수록면
- 208 - 222 (15page)
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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.
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.
목차
ABSTRACT
1. Introduction
2. Materials and methods
3. Results
4. Discussion
5. Conclusion
References
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