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红细胞膜包覆替米沙坦给药系统的纳米制备 有效增强荷瘤小鼠模型中肿瘤细胞的放射敏感性

Nanofabrications of Erythrocyte Membrane-Coated Telmisartan Delivery System Effective for Radiosensitivity of Tumor Cells in Mice Model.

机构信息

Department of Radiotherapy, the Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou Medical Center, Nanjing Medical University, Changzhou, Jiangsu, 213003, People's Republic of China.

Jiangsu Province Engineering Research Center of Medical Physics, Changzhou, Jiangsu, 213003, People's Republic of China.

出版信息

Int J Nanomedicine. 2024 Feb 16;19:1487-1508. doi: 10.2147/IJN.S441418. eCollection 2024.

DOI:10.2147/IJN.S441418
PMID:38380147
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10878400/
Abstract

BACKGROUND

Radiation stimulates the secretion of tumor stroma and induces resistance, recurrence, and metastasis of stromal-vascular tumors during radiotherapy. The proliferation and activation of tumor-associated fibroblasts (TAFs) are important reasons for the production of tumor stroma. Telmisartan (Tel) can inhibit the proliferation and activation of TAFs (resting TAFs), which may promote radiosensitization. However, Tel has a poor water solubility.

METHODS

In this study, self-assembled telmisartan nanoparticles (Tel NPs) were prepared by aqueous solvent diffusion method to solve the insoluble problem of Tel and achieve high drug loading of Tel. Then, erythrocyte membrane (ECM) obtained by hypotonic lysis was coated on the surface of Tel NPs (ECM/Tel) for the achievement of in vivo long circulation and tumor targeting. Immunofluorescence staining, western blot and other biological techniques were used to investigate the effect of ECM/Tel on TAFs activation inhibition (resting effect) and mechanisms involved. The multicellular spheroids (MCSs) model and mouse breast cancer cells (4T1) were constructed to investigate the effect of ECM/Tel on reducing stroma secretion, alleviating hypoxia, and the corresponding promoting radiosensitization effect in vitro. A mouse orthotopic 4T1 breast cancer model was constructed to investigate the radiosensitizing effect of ECM/Tel on inhibiting breast cancer growth and lung metastasis of breast cancer.

RESULTS

ECM/Tel showed good physiological stability and tumor-targeting ability. ECM/Tel could rest TAFs and reduce stroma secretion, alleviate hypoxia, and enhance penetration in tumor microenvironment. In addition, ECM/Tel arrested the cell cycle of 4T1 cells to the radiosensitive G2/M phase. In mouse orthotopic 4T1 breast cancer model, ECM/Tel played a superior role in radiosensitization and significantly inhibited lung metastasis of breast cancer.

CONCLUSION

ECM/Tel showed synergistical radiosensitization effect on both the tumor microenvironment and tumor cells, which is a promising radiosensitizer in the radiotherapy of stroma-vascular tumors.

摘要

背景

放疗会刺激肿瘤基质分泌，并在放疗过程中诱导基质-血管肿瘤的耐药性、复发和转移。肿瘤相关成纤维细胞（TAFs）的增殖和激活是产生肿瘤基质的重要原因。替米沙坦（Tel）可以抑制 TAFs 的增殖和激活（静止 TAFs），这可能促进放射增敏。然而，Tel 的水溶性较差。

方法

本研究采用水溶剂扩散法制备自组装替米沙坦纳米粒（Tel NPs），以解决 Tel 的不溶性问题并实现 Tel 的高载药量。然后，通过低渗裂解获得的红细胞膜（ECM）被包覆在 Tel NPs 的表面（ECM/Tel），以实现体内长循环和肿瘤靶向。免疫荧光染色、western blot 等生物学技术用于研究 ECM/Tel 对 TAFs 激活抑制（静止作用）及其机制。构建多细胞球体（MCSs）模型和小鼠乳腺癌细胞（4T1），以研究 ECM/Tel 在减少基质分泌、缓解缺氧以及相应促进体外放射增敏方面的作用。构建小鼠原位 4T1 乳腺癌模型，以研究 ECM/Tel 对抑制乳腺癌生长和乳腺癌肺转移的放射增敏作用。

结果

ECM/Tel 表现出良好的生理稳定性和肿瘤靶向能力。ECM/Tel 可以使 TAFs 静止，减少基质分泌，缓解缺氧，并增强肿瘤微环境中的穿透性。此外，ECM/Tel 将 4T1 细胞的细胞周期阻滞在放射敏感的 G2/M 期。在小鼠原位 4T1 乳腺癌模型中，ECM/Tel 在放射增敏方面发挥了优异的作用，显著抑制了乳腺癌的肺转移。

结论

ECM/Tel 对肿瘤微环境和肿瘤细胞均表现出协同的放射增敏作用，是一种有前途的基质-血管肿瘤放疗增敏剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e3/10878400/b724ab6e108c/IJN-19-1487-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e3/10878400/30f64d0eb952/IJN-19-1487-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e3/10878400/d087f466479b/IJN-19-1487-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e3/10878400/a540290beb73/IJN-19-1487-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e3/10878400/ba08d6078fb7/IJN-19-1487-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e3/10878400/2ac2313408b2/IJN-19-1487-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e3/10878400/338d88061625/IJN-19-1487-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e3/10878400/f2315744ca66/IJN-19-1487-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e3/10878400/b724ab6e108c/IJN-19-1487-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e3/10878400/30f64d0eb952/IJN-19-1487-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e3/10878400/d087f466479b/IJN-19-1487-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e3/10878400/a540290beb73/IJN-19-1487-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e3/10878400/ba08d6078fb7/IJN-19-1487-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e3/10878400/2ac2313408b2/IJN-19-1487-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e3/10878400/338d88061625/IJN-19-1487-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e3/10878400/f2315744ca66/IJN-19-1487-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87e3/10878400/b724ab6e108c/IJN-19-1487-g0008.jpg

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