框架

Changliu Liu, Te Tang, Hsien-Chung Lin, M. Tomizuka
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引用次数: 0

摘要

MOF纳米载体通过消耗过表达的谷胱甘肽,有效削弱细胞抗氧化能力,同时导致骨架结构分解,包被的双氢青蒿素释放。因此,被破坏的癌细胞抗氧化防御系统降低了其减轻氧化应激的作用,增强了双氢青蒿素的治疗效果。相反,正常细胞中低浓度的细胞谷胱甘肽通过减缓药物释放来保护细胞免受双氢青蒿素诱导的细胞毒性。体内实验结果表明,CMD可完全抑制小鼠肿瘤生长,无毒性迹象,为双氢青蒿素在肿瘤治疗中的实际应用提供了有效的策略。
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Framework
MOF nanocarrier of CMD can efficiently weaken the cellular antioxidant capacity by depleting the overexpressed glutathione, simultaneously leading to the decomposition of the framework structure and the release of the encapsulated dihydroartemisinin. As a result, the damaged antioxidant defense system of cancer cells reduces its effect on oxidative stress alleviation and strengthens the therapeutic efficacy of dihydroartemisinin. On contrast, the low concentration of cellular glutathione in normal cells protects them from dihydroartemisinin-induced cytotoxicity by decelerating the drug release. In vivo results demonstrate that CMD could completely suppress the tumor growth in mice and show no evidence of toxicity, providing an effective strategy for the practical usage of dihydroartemisinin in cancer therapy.
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