伊卡林通过PI3K/AKT通路准M2巨细胞极化来调节结直肠癌中的瘤微环境
Yu Chen1, Yiming Qi2, Yulan Jiang3
1School of Pharmacy, Hangzhou Normal University, Hangzhou, China; Zhejiang Key Laboratory of Disease-Syndrome Integration for Cancer Prevention and Treatment, Zhejiang Academy of Traditional Chinese Medicine, Tongde Hospital of Zhejiang Province, Hangzhou, China.
Bioorganic & medicinal chemistry
|July 19, 2025
概括
伊卡林 (ICA) 通过PI3K/AKT通路抑制M2巨分化,抑制结直肠癌 (CRC) 的进展. 这项研究强调了ICA的重点.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
- 药理学 药理学是指药理学的学科.
背景情况:
- 结肠直肠癌 (CRC) 的进展受到瘤微环境 (TME) 的影响,特别是促进瘤生长和免疫抑制的M2极化巨细胞.
- 伊卡林 (ICA) 是来自Epimedium brevicornu Maxim.的黄类化合物,已显示出潜在的抗瘤作用,但其对CRC中巨细胞介导免疫抑制的影响尚不清楚.
研究的目的:
- 为了研究伊卡林 (ICA) 在M2极化巨丰富的微环境中对结直肠癌 (CRC) 恶性瘤的影响.
- 阐明ICA调节巨细胞极化和CRC进展的基本机制.
主要方法:
- 建立了CRC细胞和M2巨细胞的共同培养系统,以评估ICA对癌细胞增殖,迁移和入侵的影响.
- 分析了M2极化标记物和PI3K/AKT通路激活,使用西斑和qRT-PCR.
- 在体内使用AOM/DSS诱导和CT26-WT同源性CRC小鼠模型验证的结果.
主要成果:
- 伊卡林 (ICA) 在与M2巨细胞共同培养时显著抑制了CRC细胞的增殖,迁移和入侵.
- ICA抑制了M2巨细胞极化,并抑制了PI3K/AKT信号通路的酸化.
- 在体内研究表明,ICA在CRC模型中减弱了瘤生长并减少了M2巨细胞透.
结论:
- 伊卡林 (ICA) 通过通过PI3K/AKT信号通路抑制M2巨分极,从而抑制结直肠癌 (CRC) 的进展.
- 这些发现揭示了ICA作用的新机制,并表明其作为治疗CRC治疗的治疗剂的潜力.
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