Chemotherapy is one of the effective ways to treat cancer because of its ability to control lesions quickly. However, chemotherapy can have many side effects due to chemotherapy indiscriminately...
Enzyme‐responsive and biocompatible supramolecular nanocarriers (NCs) have attracted intensive attention in the field of biomaterials, and have found many feasible applications, particularly for controlling drug‐release at specific anchor sites where the enzyme is overexpressed. However, the introduction of specific enzyme‐responsive sites in drug nanocarriers that can be enzymatically triggered to release drugs within tumor cells remains a challenge. In this manuscript, an enzyme‐responsive supramolecular nanoparticle, (SBE)7m‐β‐CD ⊃ PS NPs is successfully prepared, based on inducing aggregation of negatively charged cyclodextrin toward positively charged protein. The obtained nanoparticles showed trypsin‐trigger disassemble behavior that is considered as drug vehicles to load antitumor drug celastrol (CSL). Furthermore, CSL‐loaded NPs exhibit controlled release behavior of CSL in response to trypsin (TPS) stimulation. Notably, cell biology experiments reveal that loading CSL by (SBE)7m‐β‐CD ⊃ PS NPs not only reduces cytotoxicity for normal cells but also presents a similar therapeutic effect of free CSL for five tumor cells. The obtained nanoparticle appears to hold practical potential for the controllable release of CSL in tumor cells.
The pH‐responsive nanoparticles are a promising drug‐carrier because they always showed sensitivity and specificity to the pH changes caused by the surrounding environment. Most of the therapeutic drugs are generally absorbed in the stomach and small intestine due to the pH‐responsive nanoparticles always release the cargos at acidic media, making them difficult to reach the lower part of the large intestine, as well as inhibiting the therapeutic effects. Herein, an alkaline media‐sensitive supramolecular nanoparticle, regarded as SACD/PEI NPs, is prepared. SACD/PEI NPs exhibit assemble/disassemble state by changing the pH, which is used to encapsulate the anti‐colon drug CSL. CSL@SACD/PEI NPs showed a high release rate of 86.1% for the encapsulated CSL at pH = 8.5 (mimic the colon micro‐environment), while keeping stable at pH = 1.2 (mimic the gastric acid micro‐environment). Meanwhile, CSL@SACD/PEI NPs exhibited low hemolysis, indicating they possess good biocompatibility. In cell experiments, CSL@SACD/PEI NPs had a similar inhibitory effect on colon tumor cell SW480 and showed low cytotoxicity to normal cells compared with free CSL. Furthermore, both free CSL and CSL@SACD/PEI NPs showed excellent apoptosis effects on tumor cell SMMC‐7721. We hope that CSL@SACD/PEI NPs could be the valuable base‐answered drug delivery candidate, and have potential application for colon tumor therapy.
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