Oxidized low-density lipoprotein (oxLDL)-induced macrophage foam cell formation plays an important role in atherosclerosis progression. Baicalein is a constituent of Scutellaria baicalensis. Herein, we investigated the effect of baicalein on macrophage foam cell formation and the underlying mechanism. The THP-1 macrophage foam cell was established by oxLDL stimulation and the effects of baicalein on cholesterol uptake and efflux were analysed by molecular docking, ELISA, immunofluorescence, western blot, the inhibitor and siRNA experiment. The results showed that baicalein suppressed oxLDL-induced cholesterol accumulation. Mechanistically, baicalein reduced oxLDL uptake through competitive inhibiting the binding of CD36 to the epitope structure of oxLDL. Moreover, the binding of baicalein to CD36 enhanced the cholesterol efflux via the CD36-Src-JNK-ABCA1 signalling pathway. Meanwhile, Src and JNK inhibitors reversed the baicalein-induced reduction in cholesterol accumulation. In conclusion, these findings suggested that baicalein as a food supplement could inhibit macrophage foam cell formation and play an anti-atherosclerosis effect.

氧化低密度脂蛋白 (oxLDL) 诱导的巨噬细胞泡沫细胞形成在动脉粥样硬化进展中起重要作用。黄芩素是黄芩的一种成分。在此，我们研究了黄芩素对巨噬细胞泡沫细胞形成的影响及其潜在机制。oxLDL刺激建立THP-1巨噬细胞泡沫细胞，通过分子对接、ELISA、免疫荧光、western blot、抑制剂和siRNA实验分析黄芩素对胆固醇摄取和外排的影响。结果表明，黄芩素抑制了oxLDL诱导的胆固醇积累。从机制上讲，黄芩素通过竞争性抑制 CD36 与 oxLDL 表位结构的结合来减少 oxLDL 的摄取。此外，黄芩素与 CD36 的结合增强了通过 CD36-Src-JNK-ABCA1 信号通路的胆固醇流出。同时，Src 和 JNK 抑制剂逆转了黄芩素诱导的胆固醇积累减少。综上所述，