结合网络药理学探究补中益气汤抗胃癌作用及机制

Exploring the Mechanism of Buzhong Yiqi Decoction against Gastric Cancer through Network Pharmacology

  • 摘要:
    目的 评价补中益气汤(BZYQ)对胃癌(GC)的治疗作用,并阐明其潜在的作用机制。
    方法 采用小鼠胃癌移植瘤模型评价BZYQ的抗癌功效,使用HGC-27和AGS胃癌细胞系研究BZYQ对细胞迁移和侵袭的影响,通过网络药理学分析确定BZYQ治疗GC的核心分子靶点,并结合分子对接和Western blot阐明其抗癌作用的分子机制。
    结果 BZYQ能明显抑制GC移植瘤的生长。体外研究表明,BZYQ抑制HGC-27和AGS胃癌细胞的迁移和侵袭能力。BZYQ下调了PI3K/AKT信号通路中的关键蛋白AKT1,降低了EGFR蛋白表达水平,并增加了p53表达。
    结论 BZYQ在GC中的治疗作用可能涉及对PI3K/AKT通路中包括AKT1、EGFR和p53在内的靶蛋白的调节,这可能有助于确定GC治疗的新治疗靶点和策略。

     

    Abstract:
    OBJECTIVE To evaluate the therapeutic effect of Buzhong Yiqi Decoction (BZYQ) on gastric cancer (GC) and elucidate its potential mechanisms of action.
    METHODS A mouse GC xenograft model was employed to evaluate the anticancer efficacy of BZYQ. Furthermore, the impact of BZYQ on cell migration and invasion were examined in vitro using HGC-27 and AGS gastric cancer cell lines. Network pharmacology analyses were conducted to identify the core molecular targets of BZYQ in GC treatment, and molecular docking coupled with protein blotting were used to clarify the molecular mechanisms underlying its anticancer effects.
    RESULTS BZYQ clearly inhibited the growth of GC homograft tumours. In vitro studies demonstrated that BZYQ suppressed the migratory and invasive capacities of HGC-27 and AGS GC cells. Notably, BZYQ downregulated AKT1, a key protein in PI3K/AKT signaling pathway, reduced EGFR protein expression levels, and increased P53 expression.
    CONCLUSION The therapeutic effects of BZYQ in GC may involve modulation of target proteins within the PI3K/AKT pathway, including AKT1, EGFR, and P53. The findings from this study may contribute to identifying novel therapeutic targets and strategies for GC treatment.

     

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