PI3K/AKT/mTOR通路
体外
蛋白激酶B
癌症
细胞凋亡
药理学
细胞周期
机制(生物学)
癌症研究
姜辣素
化学
医学
内科学
生物化学
认识论
哲学
色谱法
作者
Jingyu Xu,Cian Zhang,Ling Wang,Meiling Wang,JIayu Liang,Yanlong Yang,Xuan Zhang
标识
DOI:10.2174/0113862073303380240722112207
摘要
Background: Precancerous Lesions of Gastric Cancer (PLGC) are critical in the secondary prevention of gastric cancer. Despite the notable effects of natural products on PLGC, the specific mechanisms by which compounds, like 6-gingerol, influence these lesions are not fully understood. Aims: This study aimed to confirm the effect and mechanism of 6-gingerol in the treatment of precancerous lesions of gastric cancer (PLGC). Objective: The objective of this study was to elucidate the effects and mechanisms of 6-gingerol against PLGC using network pharmacology and in vitro experiments. Methods: We employed network pharmacology to identify potential targets and pathways influenced by 6-gingerol, followed by validation through in vitro experiments using a PLGC cell model. Results: Network pharmacology analysis highlighted the PI3K/Akt signaling pathway as significantly influenced by 6-gingerol. In vitro experiments confirmed that 6-gingerol effectively inhibited proliferation, invasion, and metastasis of MC cells, promoted apoptosis, and induced cell cycle arrest, primarily through modulation of the PI3K/Akt pathway. Statistical analysis revealed significant inhibition (p < 0.05) across these cellular processes in a dose-dependent manner. Conclusion: This study demonstrated that 6-gingerol acts as an effective agent against PLGC, with clear dose-dependent effects that pave the way for further experimental and clinical exploration. other: none
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