Andrographis paniculata的主要活性成分Andrographolide（AG）已知可以抑制数种癌细胞的增殖。然而，其溶解度和细胞渗透性差限制了其在临床应用中的使用。在这项研究中，使用l-α磷脂酰胆碱（PC）：AG摩尔比和超声时间（ST）作为自变量，制备和优化了AG负载的植物体（AG-PTM）并确定其粒径。最佳配方为AG：PC摩尔比为1：2.7和ST为4.9分钟，粒径为243.7±7.3 nm，多分散性指数（PDI）为0.310，包封效率为72.20±4.53。该配方还显示出AG在24小时内缓慢释放的效果。研究了AG-PTMs对肝癌细胞系HepG2的抗增殖活性。AG-PTMs显著抑制了HepG2细胞的生长，IC50值为4.02±0.14 µM。在孵育该最佳配方的情况下，HepG2细胞对AG的摄取显著增强。AG-PTMs还导致G2-M期细胞周期停滞并增加了Pre-G1期细胞的凋亡分数。这些效应与氧化应激和线粒体功能障碍有关。此外，AG-PTMs显著上调了BAX的mRNA表达并下调了BCL2的mRNA表达。此外，与原始AG相比，AG-PTMs显著增强了caspase-3的浓度。这些数据表明，AG的植物体传递通过增强细胞摄取，将细胞周期阻滞在G2-M期，并诱导线粒体依赖性的凋亡显著抑制了HepG2细胞的增殖。

Andrographolide (AG), a major active constituent of Andrographis paniculata, is known to hinder proliferation of several types of cancer cells. However, its poor solubility and cellular permeability restrict its use in clinical applications. In this study, AG-loaded phytosomes (AG-PTMs) were formulated and optimized with respect to particle size using l-α-phosphatidylcholine (PC):AG ratio and sonication time (ST) as independent variables. The optimized formula was prepared at 1:2.7 for AG:PC molar ratio and 4.9 min for ST and exhibited a particle size of 243.7 ± 7.3 nm, polydispersity index (PDI) of 0.310 and entrapment efficiency of 72.20 ± 4.53. Also, the prepared formula showed a slow release of AG over 24-h period. The antiproliferative activity of AG-PTMs was investigated against the liver cancer cell line HepG2. AG-PTMs significantly repressed the growth of HepG2 cells with an IC50 value of 4.02 ± 0.14 µM. AG uptake by HepG2 cells was significantly enhanced in incubations containing the optimized formula. AG-PTMs also caused G2-M cell cycle phase arrest and increased the fraction of apoptotic cells in pre-G1 phase. These effects were associated with induction of oxidative stress and mitochondrial dysfunction. In addition, AG-PTMs significantly upregulated mRNA expression of BAX and downregulated that of BCL2. Furthermore, AG-PTMs significantly enhanced the concentration of caspase-3 in comparison to raw AG. These data indicate that the phytosomal delivery of AG significantly inhibited HepG2 cell proliferation through enhanced cellular uptake, arresting cell cycle at the G2-M phase and inducing mitochondrial-dependent apoptosis.