肝细胞癌（HCC），简称肝癌，是临床最常见的癌症之一。 HCC由于其恶性程度高、转移性强，传播范围广、发病率高。在 HCC 中，需要进一步研究阻止癌细胞迁移、侵袭和新生血管形成的有效策略。食用富含类黄酮的木蝴蝶 (OI) 具有多种有益作用，包括抗炎和抗癌特性，但其对 HCC 的潜在影响尚未得到彻底研究。在本研究中，我们旨在揭示 OI 的作用通过微流控技术研究HCC及其潜在机制。我们设计了用于细胞迁移、侵袭和新生血管形成的微流控芯片，以评估OI对HepG2细胞的影响。为了进一步探讨其抗肝癌作用机制，通过微流控芯片、RT-qPCR和免疫荧光技术研究了相关信号通路。与对照组相比，各给药组的细胞迁移、侵袭和血管生成均显着减少。根据网络药理学预测的P53和VEGF通路，进行RT-qPCR和免疫荧光染色实验。结果显示，OI上调Bax、P53和Caspase-3的表达，下调Bcl-2和MDM2的表达。据推测OI可能通过调节凋亡相关基因直接或间接诱导HepG2细胞凋亡。 OI通过下调VEGF、HIF-1α和EGFR的表达水平来阻断VEGF信号通路，抑制HepG2细胞的迁移和侵袭以及新血管的形成。我们的研究结果表明OI可能抑制HepG2细胞的迁移、侵袭和新生血管形成HepG2细胞的作用，其调节机制可能与P53和VEGF通路的调节有关。© 2023。作者。

Hepatocellular carcinoma (HCC), abbreviated as liver cancer, is one of the most common cancers in clinics. HCC has a wider spread and higher incidence due to its high malignancy and metastasis. In HCC, effective strategies to block cancer cell migration, invasion, and neovascularization need to be further studied. Consumption of flavonoid-rich Oroxylum indicum (OI) has been associated with multiple beneficial effects, including anti-inflammatory and anticancer properties, but the potential effects on HCC have not been thoroughly investigated.In this study, we aimed to reveal the effect of OI on HCC and its potential mechanism through microfluidic technology.We designed microfluidic chips for cell migration, invasion, and neovascularization to evaluate the effect of OI on HepG2 cells. To further explore the mechanism of its anti-liver cancer action, the relevant signaling pathways were studied by microfluidic chips, RT‒qPCR and immunofluorescence techniques. Compared to the control group, cell migration, invasion, and angiogenesis were significantly reduced in each administration group. According to the P53 and VEGF pathways predicted by network pharmacology, RT‒qPCR and immunofluorescence staining experiments were conducted.The results showed that OI upregulated the expression of Bax, P53 and Caspase-3 and downregulated the expression of Bcl-2 and MDM2. It has been speculated that OI may directly or indirectly induce apoptosis of HepG2 cells by regulating apoptosis-related genes. OI blocks the VEGF signaling pathway by downregulating the expression levels of VEGF, HIF-1α and EGFR and inhibits the migration and invasion of HepG2 cells and the formation of new blood vessels.Our findings suggest that OI may inhibit the migration, invasion, and neovascularization of HepG2 cells, and its regulatory mechanism may be related to the regulation of the P53 and VEGF pathways.© 2023. The Author(s).