研究磁性 Fe3O4 纳米颗粒介导的藤黄酸对 Capan-1 胰腺癌细胞抗癌功效的增强作用。

Study of the enhanced anticancer efficacy of gambogic acid on Capan-1 pancreatic cancer cells when mediated via magnetic Fe3O4 nanoparticles.

机构信息

Department of Oncology, Zhongda Hospital, Medical School, Southeast University, Nanjing, People's Republic of China.

出版信息

Int J Nanomedicine. 2011;6:1929-35. doi: 10.2147/IJN.S24707. Epub 2011 Sep 9.

DOI:10.2147/IJN.S24707

PMID:21931488

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3173055/

Abstract

BACKGROUND

Gambogic acid (GA), a potent anticancer agent, is limited in clinical administration due to its poor water solubility. The aim of this study was to explore a drug delivery system based on magnetic Fe(3)O(4) nanoparticles (MNP-Fe(3)O(4)) conjugated with GA to increase water solubility of the drug and enhance its chemotherapeutic efficiency for pancreatic cancer.

METHODS

GA was conjugated with the MNP-Fe(3)O(4) colloidal suspension by mechanical absorption polymerization to construct GA-loaded MNP-Fe(3)O(4), which acted as a drug delivery system.

RESULTS

Combination therapy with GA and MNP-Fe(3)O(4) induced remarkable improvement in anticancer activity, which was demonstrated by optical microscopic observations, MTT assay, and nuclear DAPI staining. Furthermore, the possible signaling pathway was explored by Western blot. In Capan-1 pancreatic cancer cells, our observations demonstrated that this strategy could enhance potential anticancer efficiency by inducing apoptosis. The mechanisms of the synergistic effect may be due to reducing protein expression of Bcl-2 and enhancing that of Bax, caspase 9, and caspase 3.

CONCLUSION

These findings demonstrate that a combination of GA and MNPs-Fe(3)O(4) represents a promising approach to the treatment of pancreatic cancer.

摘要

背景

由于 Gambogic 酸（GA）的水溶性差，其作为一种有效的抗癌药物，在临床应用中受到限制。本研究旨在探索一种基于磁性 Fe（3）O（4）纳米粒子（MNP-Fe（3）O（4））的药物传递系统，将 GA 与该系统结合以增加药物的水溶性，并增强其对胰腺癌的化疗效果。

方法

通过机械吸收聚合将 GA 与 MNP-Fe（3）O（4）胶体悬浮液结合，构建负载 GA 的 MNP-Fe（3）O（4），作为药物传递系统。

结果

GA 和 MNP-Fe（3）O（4）联合治疗显著提高了抗癌活性，这通过光学显微镜观察、MTT 测定和核 DAPI 染色得到证实。此外，通过 Western blot 探索了可能的信号通路。在 Capan-1 胰腺癌细胞中，我们的观察表明，这种策略可以通过诱导细胞凋亡来增强潜在的抗癌效率。协同作用的机制可能是由于降低了 Bcl-2 的蛋白表达，增强了 Bax、caspase 9 和 caspase 3 的表达。