与卵巢癌相关的显着死亡率强调了该领域迫切需要新的治疗干预措施。本研究的重点是评估 auraptene 纳米杂化壳聚糖叶酸对 A2780 卵巢癌细胞的细胞毒性影响。使用液体和固体脂质的组合来创建auaptene纳米结构脂质载体。将叶酸与壳聚糖结合以修饰表面。将含有亚甲基蓝的纳米颗粒溶解在去离子蒸馏水中，以将壳聚糖-叶酸附着到纳米颗粒上。采用刃天青细胞活力测定来测量aurapten对细胞的细胞毒性。利用实时 PCR 定量 Bcl-2、Bax 和 P53 基因的表达水平。 DLS 分析显示出直径约为 211 nm 的球形颗粒。在对癌细胞 (A2780) 有毒的浓度下，aurapten 纳米颗粒并未表现出对正常细胞系 (HFF-1) 的抑制作用。体外试验表明，aurapten 纳米粒子通过促进促凋亡基因（Bax 和 P53）的表达，同时抑制抗凋亡基因（Bcl-2）的表达，以剂量响应的方式触发 A2780 细胞凋亡。此外，aurapten 纳米颗粒还增加了癌细胞内活性氧的产生。 auraptene 纳米粒子对人类卵巢癌的显着细胞毒性和致命影响可能归因于它们产生氧化应激条件并诱导细胞凋亡的能力。© 2024。作者获得 Springer-Verlag GmbH 德国（Springer 旗下公司）的独家许可自然。

The significant fatality rate associated with ovarian cancer underscores the urgent need for novel therapeutic interventions in this area. The focus of this study was to assess the cytotoxic impact of auraptene nanohybrid chitosan folate on A2780 ovarian cancer cells. A combination of liquid and solid lipids were used to create auraptene-nanostructured lipid carriers. Folic acid was conjugated to chitosan in order to modify the surface. The nanoparticles containing methylene blue were dissolved in deionized distilled water to attach the chitosan-folic acid to the nanoparticles. The resazurin cell viability assay was employed to gauge the cytotoxicity of auraptene on the cells. Real-time PCR was utilized to quantify the expression levels of Bcl-2, Bax, and P53 genes. DLS analysis exposed a spheroidal particle with an approximate diameter of 211 nm. The auraptene nanoparticles did not revealed inhibitory effect on normal cell line (HFF-1) at the concentrations that it was toxic for cancerous cells (A2780). In vitro trials suggested that auraptene nanoparticles trigger apoptosis in A2780 cells in a dose-responsive manner by promoting the expression of pro-apoptotic genes (Bax and P53), while suppressing the expression of the anti-apoptotic gene (Bcl-2). Furthermore, auraptene nanoparticles also heightened the production of reactive oxygen species within the cancerous cells. The notable cytotoxic and lethal influence of auraptene nanoparticles on human ovarian cancer may be attributed to their capacity to generate oxidative stress conditions and induce apoptosis.© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.