肝细胞癌（HCC）是一种常见且致命的恶性肿瘤。传统中药，例如复方黄芪（野生黄芩苷），已显示出改善肝癌患者预后的希望。本研究旨在探讨野生黄芩苷对人肝癌细胞系HepG2的影响并阐明其潜在机制，特别是AKR1B10和PI3K/AKT信号通路的作用。用不同浓度的野生黄芩苷处理HepG2细胞。分别使用 CCK-8、流式细胞术、划痕、Transwell 和克隆形成实验评估细胞增殖、凋亡、迁移、侵袭和细胞周期。进行转录组测序来分析野生黄芩苷诱导的基因表达变化。使用基因本体论（GO）和京都基因和基因组百科全书（KEGG）途径富集分析来鉴定和分析差异表达的基因。通过qPCR验证AKR1B10和PI3K的表达。野生黄芩苷以剂量依赖性方式抑制HepG2细胞增殖，诱导细胞凋亡，抑制迁移和侵袭，并导致细胞周期停滞。转录组测序发现1202个差异表达基因，其中上调基因486个，下调基因716个。 GO分析表明，生物过程在野生黄芩苷的抗癌机制中至关重要，而KEGG分析则确定代谢途径是最受调节的。 qPCR证实野生黄芩苷下调代谢途径关键基因AKR1B10和PI3K。研究结果表明，野生黄芩苷通过诱导细胞凋亡，抑制增殖、迁移和侵袭，使细胞凋亡，从而对HepG2细胞表现出有效的抗癌作用。循环逮捕。野生黄芩苷对 AKR1B10 和 PI3K/AKT 信号通路的调节作用似乎对其抑制 HCC 细胞增殖的作用至关重要。这些结果为野生黄芩苷的作用机制提供了新的见解，并支持其作为 HCC 治疗方法的潜力。© 2024 Sun 等人。

Hepatocellular carcinoma (HCC) is a common and deadly malignancy. Traditional Chinese medicine, such as the compound Astragalus (wild Baicalin), has shown promise in improving outcomes for HCC patients. This study aimed to investigate the effects of wild Baicalin on the human hepatoma cell line HepG2 and elucidate the underlying mechanisms, particularly the role of the AKR1B10 and PI3K/AKT signaling pathways.HepG2 cells were treated with varying concentrations of wild Baicalin. Cell proliferation, apoptosis, migration, invasion, and cell cycle were evaluated using CCK-8, flow cytometry, scratch, Transwell, and clonogenic assays, respectively. Transcriptome sequencing was performed to analyze gene expression changes induced by wild Baicalin. Differentially expressed genes were identified and analyzed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. The expression of AKR1B10 and PI3K was validated by qPCR.Wild Baicalin inhibited HepG2 cell proliferation, induced apoptosis, suppressed migration and invasion, and caused cell cycle arrest in a dose-dependent manner. Transcriptome sequencing revealed 1202 differentially expressed genes, including 486 upregulated and 716 downregulated genes. GO analysis indicated that biological processes were pivotal in the anticancer mechanism of wild Baicalin, while KEGG analysis identified metabolic pathways as the most significantly regulated. AKR1B10 and PI3K, key genes in metabolic pathways, were downregulated by wild Baicalin, which was confirmed by qPCR.The findings suggest that wild Baicalin exhibits potent anticancer effects against HepG2 cells by inducing apoptosis, inhibiting proliferation, migration, and invasion, and causing cell cycle arrest. The regulatory effects of wild Baicalin on the AKR1B10 and PI3K/AKT signaling pathways appear to be critical for its inhibitory effects on HCC cell proliferation. These results provide new insights into the mechanism of action of wild Baicalin and support its potential as a therapeutic approach for HCC treatment.© 2024 Sun et al.