Nuciferine, a main bioactive component obtained from the lotus leaf, is an antagonist at 5-HT2A, 5-HT2C, and 5-HT2B receptors, with the IC50 values of 0.478μM, 0.131μM, and 1μM, respectively[1]. Nuciferine can reduce blood lipids by inhibiting cholesterol synthesis and cholesterol esterase activity, and increasing the expression of low-density lipoprotein receptor[2]. Nuciferine has been widely used to reduce serum uric acid levels, improve renal function, and as a key anti-inflammatory compound in mouse models of hyperuricemia[3].
In vitro, Nuciferine treatment for 72 hours significantly inhibited the proliferation of HepG2 cells and HCCLM3 cells, with IC50 values of 67.97μM and 61.88μM, respectively[4]. Treatment of 3T3-L1 preadipocytes with 20μM Nuciferine for 72 hours significantly inhibited cell proliferation, reduced intracellular lipid accumulation, decreased triglyceride content, and down-regulated the expression of lipid metabolism-related genes[5]. Treatment of chondrocytes with 25μM Nuciferine for 24h significantly reduced IL-1β-induced iNOS, PEG2 and IL-6 levels in mouse chondrocytes, significantly reduced IL-1β-induced degradation of extracellular matrix, without affecting cell viability[6].
In vivo, Nuciferine treatment (400mg/kg/day) via oral administration for 42 days resulted in a significant reduction in both plasma and hepatic triglyceride concentrations and a significant increase in hepatic glycogen content in male broiler chickens[7]. Intraperitoneal injection of Nuciferine (20mg/kg) every 2 days for 2 weeks significantly suppressed the volume and weight of the suppressed tumor in the xenograft tumor mouse models[8].
References:
[1] Farrell M S, McCorvy J D, Huang X P, et al. In vitro and in vivo characterization of the alkaloid nuciferine[J]. PLoS One, 2016, 11(3): e0150602.
[2] Huang X, Hao N, Chen G, et al. Chemistry and biology of nuciferine[J]. Industrial Crops and Products, 2022, 179: 114694.
[3] Wang M X, Liu Y L, Yang Y, et al. Nuciferine restores potassium oxonate-induced hyperuricemia and kidney inflammation in mice[J]. European Journal of Pharmacology, 2015, 747: 59-70.
[4] Li T, Wang W, Zhu M, et al. The antineoplastic effects of nuciferine on hepatocellular carcinoma are associated with suppression of the HER2-AKT/ERK1/2 signaling pathway[J]. Discover Oncology, 2025, 16(1): 822.
[5] Xu H, Wang L, Yan K, et al. Nuciferine inhibited the differentiation and lipid accumulation of 3T3-L1 preadipocytes by regulating the expression of lipogenic genes and adipokines[J]. Frontiers in Pharmacology, 2021, 12: 632236.
[6] Peng M, Shen G, Tu Q, et al. Nuciferine ameliorates osteoarthritis: An in vitro and in vivo study[J]. International Immunopharmacology, 2024, 142: 113098.
[7] Zhou Y, Chen Z, Lin Q, et al. Nuciferine reduced fat deposition by controlling triglyceride and cholesterol concentration in broiler chickens[J]. Poultry Science, 2020, 99(12): 7101-7108.
[8] Xie J R, Chen X J, Zhou G. Nuciferine inhibits oral squamous cell carcinoma partially through suppressing the STAT3 signaling pathway[J]. International Journal of Molecular Sciences, 2023, 24(19): 14532.
Nuciferine是从荷叶中提取的主要生物活性成分，可作为5-HT2A、5-HT2C和5-HT2B受体拮抗剂，IC50值分别为0.478μM、0.131μM和1μM[1]。Nuciferine通过抑制胆固醇合成和胆固醇酯酶活性，并增加低密度脂蛋白受体表达来降低血脂[2]。Nuciferine广泛用于高尿酸血症小鼠模型中以降低血清尿酸水平、改善肾功能，并作为关键抗炎化合物[3]。
在体外，Nuciferine处理72小时可显著抑制HepG2和HCCLM3细胞增殖，IC50值分别为67.97μM和61.88μM[4]。20μM的Nuciferine处理3T3-L1前脂肪细胞72小时能显著抑制细胞增殖、减少细胞内脂质积累、降低甘油三酯含量，并下调脂代谢相关基因表达[5]。25μM的Nuciferine处理小鼠软骨细胞24小时可显著降低IL-1β诱导的iNOS、PEG2和IL-6水平，显著抑制IL-1β诱导的细胞外基质降解，不影响细胞活力[6]。
在体内，雄性肉鸡经口服Nuciferine（400mg/kg/day，持续42天）后，血浆和肝脏甘油三酯浓度显著降低，肝糖原含量显著增加[7]。异种移植瘤小鼠模型经腹腔注射Nuciferine（20mg/kg，每2天一次，持续2周）后，肿瘤体积和肿瘤重量均被显著抑制[8]。