Emodin (EM) is one of the active components of the traditional Chinese medicine rhubarb, and there is evidence of its hypolipidemic activity, though the exact mechanism is unknown. NPC1L1 is a key protein in human cholesterol uptake that is primarily expressed in hepatocytes and gastrointestinal epithelial cells. Our findings suggest that rhodopsin inhibits cellular cholesterol uptake by influencing NPC1L1 cholesterol transport. The results showed that NBD-cholesterol uptake in human HepG2 cells was 27 %, 31.3 %, 33.6 %, 41.6 %, and 52.6 % of control after treatment with 100, 75, 50, 25, and 12.5 % M EM, respectively, compared to 50 % for 100 M Ezetimibe. Kinetic studies revealed that EM inhibited cellular uptake of cholesterol through anti-competitive inhibition. Furthermore, using confocal fluorescence quantification, we discovered that after cholesterol deprivation treatment reintroduced cholesterol supply, cholesterol uptake was significantly higher in HepG2 cells highly expressing NPC1L1 than in U2OS cells with low NPC1L1 expression. As a result, we hypothesize that EM may inhibit cholesterol uptake via NPC1L1 in human hepatocytes in an anti-competitive manner. Overall, as a dietary supplement or lipid-modifying drug, EM has the potential to lower cholesterol.

大黄素（EM）是中药大黄的活性成分之一，有证据表明其具有降血脂作用，但具体机制尚不清楚。NPC1L1 是人类胆固醇摄取的关键蛋白，主要在肝细胞和胃肠道上皮细胞中表达。我们的研究结果表明，视紫红质通过影响 NPC1L1 胆固醇转运来抑制细胞胆固醇摄取。结果显示，在用 100、75、50、25 和 12.5 % M EM 处理后，人 HepG2 细胞中的 NBD-胆固醇摄取分别为对照的 27 %、31.3 %、33.6 %、41.6 和 52.6 %，与对于 100 M 依折麦布，为 50 %。动力学研究表明，EM 通过反竞争抑制来抑制细胞对胆固醇的摄取。此外，使用共焦荧光定量，我们发现，在胆固醇剥夺治疗重新引入胆固醇供应后，高表达 NPC1L1 的 HepG2 细胞中的胆固醇摄取显着高于低表达 NPC1L1 的 U2OS 细胞。因此，我们假设 EM 可能以反竞争的方式抑制人肝细胞中 NPC1L1 对胆固醇的摄取。总体而言，作为膳食补充剂或调脂药物，EM 具有降低胆固醇的潜力。