Changliu Liu, Te Tang, Hsien-Chung Lin, M. Tomizuka
{"title":"Framework","authors":"Changliu Liu, Te Tang, Hsien-Chung Lin, M. Tomizuka","doi":"10.18356/6ec4b733-en","DOIUrl":null,"url":null,"abstract":"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.","PeriodicalId":299675,"journal":{"name":"DANCE, ARCHITECTURE AND ENGINEERING","volume":"15 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2018-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"DANCE, ARCHITECTURE AND ENGINEERING","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.18356/6ec4b733-en","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
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.