As a natural product with various biological activities, triptolide (TP) has been reported in anti-inflammatory, anti-tumor and anti-autoimmune studies. However, the narrow therapeutic window, poor water solubility, and fast metabolism limit its wide clinical application. To reduce its adverse effects and enhance its efficacy, research and design of targeted drug delivery systems (TDDS) based on nanomaterials is one of the most viable strategies at present. This review summarizes the reports and studies of TDDS combined with TP in recent years, including passive and active targeting of drug delivery systems, and specific delivery system strategies such as polymeric micelles, solid lipid nanoparticles, liposomes, and stimulus-responsive polymer nanoparticles. The reviewed literature presented herein indicates that TDDS is a multifunctional and efficient method for the delivery of TP. In addition, the advantages and disadvantages of TDDS are sorted out, aiming to provide reference for the combination of traditional Chinese medicine and advanced nano drug delivery systems (NDDS) in the future.
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A biobased epoxy monomer (GA-II) derived from gallic acid for multiwalls carbon nanotubes' (MWCNTs) dispersion improvement is reported in this article. The aromatic group in its molecular structure made it to be absorbed onto the surface of MWCNTs via p-p interactions and the GA-II anchored MWCNT could be homogeneously dispersed in DGEBA matrix via sonication. That was proved by Raman and UV spectroscopy as well as scanning electron microscope. After curing reaction, the epoxy/MWCNT composites demonstrated enhanced mechanical properties, excellent thermal conductivity, and high electrical conductivity. With the addition of only 0.5 wt% GA-II modified MWCNT, the tensile strength, tensile modulus, flexural strength, and flexural modulus of the composites were improved by 28%, 40%, 22%, and 16%, respectively. The thermal and electrical conductivities were also improved from 0.15 to 0.25 W/m K (67% increased) and from 0.7 3 10 214 to 0.24 3 10 24 S cm 21 (10 orders increased)
Background: Up to 80% of pancreatic cancer patients suffer from cachexia. White adipose tissue (WAT) browning caused by the tumorigenicity and progression aggravates the cancer-associated cachexia (CAC). Cancer-initiated changes in the protein-38 mitogen-activated protein kinases (p38 MAPK) pathway are likely involved in the development of CAC. Methods: p38 MAPK inhibitors, VCP979 or SB203580, were used in the in vitro and in vivo models of pancreatic cancer cachexia. Expression of uncoupling protein 1 (UCP1) in the p38 MARK pathway and the properties and level of white adipocytes were analyzed and correlated to browning, followed by immunohistochemistry and Western blotting validations. Changes in the volume and fat fraction of WAT in animals were monitored by magnetic resonance imaging (MRI). Results: The size of white adipocytes was increased after being treated with the p38 MAPK inhibitors, along with increase in the MRI-measured volume and fat fraction of WAT. Comparing two p38 MAPK inhibitors, the p38α subunit-specific inhibitor VCP979 had a better therapeutic effect than SB203580, which targets both p38α and β subunits. Conclusions: Blockade of p38 MAPK reduced the WAT browning that contributes to CAC. Thus, p38 MARK inhibitors can potentially be used as a therapy for treating CAC. Non-invasive MRI can also be applied to assess the progression and treatment responses of CAC.
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