Tea nanoparticle, a safe and biocompatible nanocarrier, greatly potentiates the anticancer activity of doxorubicin
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Yi-Jun Wang1, Yujian Huang2, Nagaraju Anreddy1, Guan-Nan Zhang1, Yun-Kai Zhang1, Meina Xie1, Derrick Lin2, Dong-Hua Yang1, Mingjun Zhang2, Zhe-Sheng Chen1
1Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John’s University, Queens, NY 11439, USA
2Department of Biomedical Engineering, College of Engineering, The Ohio State University, Columbus, OH 43210, USA
Zhe-Sheng Chen, e-mail: firstname.lastname@example.org
Mingjun Zhang, e-mail: email@example.com
Keywords: tea nanoparticle, tumor xenograft, multidrug resistance, drug delivery, biocompatibility
Received: September 02, 2015 Accepted: November 25, 2015 Published: December 21, 2015
An infusion-dialysis based procedure has been developed as an approach to isolate organic nanoparticles from green tea. Tea nanoparticle (TNP) can effectively load doxorubicin (DOX) via electrostatic and hydrophobic interactions. We established an ABCB1 overexpressing tumor xenograft mouse model to investigate whether TNP can effectively deliver DOX into tumors and bypass the efflux function of the ABCB1 transporter, thereby increasing the intratumoral accumulation of DOX and potentiating the anticancer activity of DOX. MTT assays suggested that DOX-TNP showed higher cytotoxicity toward CCD-18Co, SW620 and SW620/Ad300 cells than DOX. Animal study revealed that DOX-TNP resulted in greater inhibitory effects on the growth of SW620 and SW620/Ad300 tumors than DOX. In pharmacokinetics study, DOX-TNP greatly increased the SW620 and SW620/Ad300 intratumoral concentrations of DOX. But DOX-TNP had no effect on the plasma concentrations of DOX. Furthermore, TNP is a safe nanocarrier with excellent biocompatibility and minimal toxicity. Ex vivo IHC analysis of SW620 and SW620/Ad300 tumor sections revealed evidence of prominent antitumor activity of DOX-TNP. In conclusion, our findings suggested that natural nanomaterials could be useful in combating multidrug resistance (MDR) in cancer cells and potentiating the anticancer activity of chemotherapeutic agents in cancer treatment.
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