Zlotnikov Igor D, Ezhov Alexander A, Dobryakova Natalia V, Kudryashova Elena V
Faculty of Chemistry, Lomonosov Moscow State University, Leninskie Gory, 1/3, 119991 Moscow, Russia.
Faculty of Physics, Lomonosov Moscow State University, Leninskie Gory, 1/2, 119991 Moscow, Russia.
Gels. 2024 Feb 20;10(3):157. doi: 10.3390/gels10030157.
We have developed a micellar formulation of anticancer drugs based on chitosan and heparin grafted with lipoic and oleic acids that can release the cytotoxic cargo (doxorubicin) in response to external stimuli, such as increased glutathione concentration-a hallmark of cancer. Natural polysaccharides (heparin and chitosan) provide the pH sensitivity of the nanocarrier: the release of doxorubicin (Dox) is enhanced in a slightly acidic environment (tumor microenvironment). Fatty acid residues are necessary for the formation of nanoparticles (micelles) and solubilization of cytostatics in a hydrophobic core. Lipoic acid residues provide the formation of a labile S-S cross-linking between polymer chains (the first variant) or covalently attached doxorubicin molecules through glutathione-sensitive S-S bridges (the second variant)-both determine Redox sensitivity of the anticancer drugs carriers stable in blood circulation and disintegrate after intracellular uptake in the tumor cells. The release of doxorubicin from micelles occurs slowly (20%/6 h) in an environment with a pH of 7.4 and the absence of glutathione, while in a slightly acidic environment and in the presence of 10 mM glutathione, the rate increases up to 6 times, with an increase in the effective concentration up to 5 times after 7 h. The permeability of doxorubicin in micellar formulations (covalent S-S cross-linked and not) into Raji, K562, and A875 cancer cells was studied using FTIR, fluorescence spectroscopy and confocal laser scanning microscopy (CLSM). We have shown dramatically improved accumulation, decreased efflux, and increased cytotoxicity compared to doxorubicin control with three tumor cell lines: Raji, K562, and A875. At the same time, cytotoxicity and permeability for non-tumor cells (HEK293T) are significantly lower, increasing the selectivity index against tumor cells by several times.
我们研发了一种基于壳聚糖和肝素的抗癌药物胶束制剂,壳聚糖和肝素接枝了硫辛酸和油酸,该制剂能够响应外部刺激(如谷胱甘肽浓度升高——癌症的一个标志)释放细胞毒性药物(阿霉素)。天然多糖(肝素和壳聚糖)赋予了纳米载体pH敏感性:在略酸性环境(肿瘤微环境)中阿霉素(Dox)的释放会增强。脂肪酸残基对于纳米颗粒(胶束)的形成以及细胞抑制剂在疏水核中的溶解是必需的。硫辛酸残基可在聚合物链之间形成不稳定的S-S交联(第一种变体),或通过谷胱甘肽敏感的S-S桥与共价连接的阿霉素分子形成交联(第二种变体)——这两种情况都决定了抗癌药物载体在血液循环中稳定且在肿瘤细胞内摄取后分解的氧化还原敏感性。在pH为7.4且无谷胱甘肽的环境中,阿霉素从胶束中的释放缓慢(20%/6小时),而在略酸性环境且存在10 mM谷胱甘肽的情况下,释放速率提高至6倍,7小时后有效浓度提高至5倍。使用傅里叶变换红外光谱(FTIR)、荧光光谱和共聚焦激光扫描显微镜(CLSM)研究了胶束制剂(共价S-S交联和非共价S-S交联)中阿霉素对Raji、K562和A875癌细胞的渗透性。与阿霉素对照相比,我们发现对于三种肿瘤细胞系Raji、K562和A875,阿霉素在胶束制剂中的积累显著改善、外排减少且细胞毒性增加。同时,对非肿瘤细胞(HEK293T)的细胞毒性和渗透性显著更低,使针对肿瘤细胞的选择性指数提高了数倍。