目的 探究姜黄素通过调节Toll样受体4/核转录因子⁃κB（TLR4/NF⁃κB）信号通路，抑制人肾细胞癌（RCC）恶性表型。方 法 将体外培养的HK⁃2、786⁃0、ACHN细胞株分为对照组、姜黄素组、TLR4/NF⁃κB信号通路抑制剂组（瑞沙托维，TAK⁃242组），其中 姜黄素组依据不同干预剂量分为姜黄素10、20、40 μmol/L亚组。CCK⁃8法、Annexin V⁃FITC/碘化丙啶染色、划痕实验、Transwell小室 实验分别检测细胞增殖、凋亡、迁移、侵袭能力；ELISA法检测细胞白介素⁃1β（IL⁃1β）、白介素⁃6（IL⁃6）和肿瘤坏死因子⁃α（TNF⁃α）含 量；蛋白印迹法检测TLR4、NF⁃κB p65、B细胞淋巴瘤⁃2（Bcl⁃2）、Bcl⁃2相关X的蛋白质（Bax）、基质金属蛋白酶9（MMP⁃9）的表达。结 果 姜黄素在40 μmol/L以下浓度时不存在毒性作用；在RCC细胞株786⁃0、ACHN中，与对照组相比，姜黄素10、20、40 μmol/L亚组能 够明显抑制细胞增殖、迁移和侵袭，促进细胞凋亡；IL⁃1β、IL⁃6和TNF⁃α、TLR4、NF⁃κB p65、Bcl⁃2、MMP⁃9水平降低，Bax水平升高，差 异均有统计学意义（均P<0.05）。结论 姜黄素可通过抑制TLR4/NF⁃κB信号通路，抑制RCC细胞的增殖、迁移和侵袭，并促进细胞凋亡。

Objective To explore curcumin inhibiting the malignant phenotype of human renal cell carcinoma (RCC) by regulating the Toll⁃like receptor 4/nuclear factor⁃κB (TLR4/NF⁃κB) signaling pathway. Method The HK⁃2, 786⁃0, and ACHN cell lines cultured in vitro were divided into control group, curcumin group, TLR4/NF⁃κB signaling pathway inhibitor group (TAK⁃242 group). The curcumin group was divided into curcumin 10, 20, 40 μmol/L subgroup. CCK⁃8 method, Annexin V⁃FITC/PI staining, scratch test, and Transwell chamber test were used to detect ability of cell proliferation, apoptosis, migration and invasion; ELISA method was used to detect cell interleukin⁃1β (IL⁃1β), interleukin⁃6 (IL⁃6) and tumor necrosis factor⁃α (TNF⁃α) content; Western blotting method was used to detect the expression of TLR4, NF⁃κB p65, B cell lymphoma⁃2 (Bcl⁃2), BCL2⁃Associated X (Bax), and matrix metalloprotein⁃9 (MMP⁃9). Result Curcumin had no toxic effect at concentrations below 40 μmol/L; in renal cancer cell lines 786⁃0 and ACHN, Compared with the control group, curcumin 10, 20, and 40 μmol/L subgroups can significantly inhibit cell proliferation, migration and invasion, and promote cell apoptosis; IL⁃1β, IL⁃6 and TNF⁃α, TLR4, NF⁃κB p65, Bcl⁃2, MMP⁃9 levels decrease, and Bax levels increase, The differences are statistically significant (P<0.05). Conclusion Curcumin can inhibit the proliferation, migration and invasion of renal cancer cells and promote cell apoptosis by inhibiting the TLR4/NF⁃κB signaling pathway.