探讨红花黄（SY）对肝细胞癌（HCC）的抗肿瘤作用及其潜在机制。通过混合Luc-Hepa1-6细胞和CD3 CD8 T细胞，然后添加程序化细胞建立体外模型死亡蛋白 1 (PD-1) 抗体（抗 mPD-1），带或不带 SY。流式细胞术检测细胞凋亡，酶联免疫吸附法测定炎症细胞因子水平。通过Western blot检测程序性细胞死亡1配体1（PD-L1）、趋化因子配体（CCL5）、C-X-C基序趋化因子配体10（CXCL10）的蛋白水平。在小鼠中建立原位动物模型，然后用抗 mPD-1 联合或不联合 SY 进行治疗。使用 AniView 100 成像系统监测生物发光成像。为了建立 FAK 过表达的 Luc-Hepa1-6 细胞，用含有 pcDNA3.1-FAK 的腺病毒转染细胞 48 小时。 -mPD-1 (P<0.01)，伴随着 PD-1/PD-L1 轴的失活，SY 进一步增强了这种失活 (P<0.05 或 P<0.01)。在抗 mPD-1 处理的小鼠中观察到荧光强度增加、CD3 CD8 T 细胞百分比升高、促进炎症细胞因子的释放、PD-1/PD-L1 轴失活以及 CCL5/CXCL10 分泌增加 (P<0.01)。 SY 显着增强了这些结果（P<0.05 或 P<0.01）。此外，在抗 mPD-1 处理的 Luc-Hepa1 混合物中，SY 对抑制肿瘤细胞生长、促进细胞凋亡和炎症细胞因子释放、抑制 PD-1/PD-L1 轴以及诱导 CCL5/CXCL10 分泌的增强作用-6 细胞和 CD3 CD8 T 细胞因 FAK 过表达而被消除（P<0.01）。SY 通过抑制 FAK 介导免疫耐受，从而抑制 HCC 的进展。© 2023。中华中西医结合杂志出版社和 Springer-Verlag GmbH 德国，隶属于施普林格自然集团。

To explore the anti-tumor effect of safflower yellow (SY) against hepatocellular carcinoma (HCC) and the underlying potential mechanism.An in vitro model was established by mixing Luc-Hepa1-6 cells and CD3+CD8+ T cells, followed by adding programmed cell death protein 1 (PD-1) antibody (Anti-mPD-1) with or without SY. The apoptosis was detected by flow cytometry and the level of inflammatory cytokines was determined by enzyme-linked immunosorbent assay. The protein levels of programmed cell death 1 ligand 1 (PD-L1), chemokine ligand (CCL5), C-X-C motif chemokine ligand 10 (CXCL10) were measured by Western blot. An in situ animal model was established in mice followed by treatment with anti-mPD-1 with or without SY. Bioluminescence imaging was monitored with an AniView 100 imaging system. To establish the FAK-overexpressed Luc-Hepa1-6 cells, cells were transfected with adenovirus containing pcDNA3.1-FAK for 48 h.The fluorescence intensity, apoptotic rate, release of inflammatory cytokines, and CCL5/CXCL10 secretion were dramatically facilitated by anti-mPD-1 (P<0.01), accompanied by an inactivation of PD-1/PD-L1 axis, which were extremely further enhanced by SY (P<0.05 or P<0.01). Increased fluorescence intensity, elevated percentage of CD3+CD8+ T cells, facilitated release of inflammatory cytokines, inactivated PD-1/PD-L1 axis, and increased CCL5/CXCL10 secretion were observed in Anti-mPD-1 treated mice (P<0.01), which were markedly enhanced by SY (P<0.05 or P<0.01). Furthermore, the enhanced effects of SY on inhibiting tumor cell growth, facilitating apoptosis and inflammatory cytokine releasing, suppressing the PD-1/PD-L1 axis, and inducing the CCL5/CXCL10 secretion in Anti-mPD-1 treated mixture of Luc-Hepa1-6 cells and CD3+CD8+ T cells were abolished by FAK overexpression (P<0.01).SY inhibited the progression of HCC by mediating immunological tolerance through inhibiting FAK.© 2023. The Chinese Journal of Integrated Traditional and Western Medicine Press and Springer-Verlag GmbH Germany, part of Springer Nature.