PLGA nanoparticles of a new cinnamic acid derivative inhibits cellular proliferation on breast cancer cell line MCF-7 in a PPARγ dependent way.

Currently, cancer treatments are highly invasive, and they have been associated with a lot of adverse effects that put patient integrity at risk. Therefore, research of novel molecules and delivery systems capable of achieving a therapeutic effect that modifies inhibits and reduces the proliferative activity in cancer cells and, at the same time, reduce adverse effects associated with conventional therapies is imperative. In this study, we analyzed the biological effect of a novel cinnamic acid derivative, 3,4-dichlorobencil-p-phenoxylcilamide, in polymeric nanoparticles over MCF-7 breast cancer cells. The nanoparticulated system showed an inhibitory influence over cellular metabolism at equal or higher concentrations than 25 µM of 3,4-dichlorobencil-p-phenoxylcilamide, which is associated with PPARγ transcriptional activity, in addition to the decrease in the proliferation antigen Ki-67 basal levels. Those results position this kind of nanoscale system as an alternative on breast cancer treatment and lay the basis for research on the action mechanism associated with its cellular metabolism modulation and relationship with another hallmark on breast cancer cellular models.

Oxidative stress modulation induced by chitosan-glutathione nanoparticles in chondrocytes.

The use of nanometric systems to deliver biologically active substances is a successful tool in different fields. In this study, we investigated nanometric systems with antioxidant capacity to modulate events associated with the redox state in human chondrocytes. We used nanoparticles (NPs) prepared with chitosan and glutathione (GSH) and an in vitro model: primary cultures of human chondrocytes were extracted from hyaline cartilage. The cells were exposed to CdCl2 in the presence or absence of NPs. CdCl2 is a widely known oxidizing agent. Fluorescence and confocal microscopy showed the location of the NPs within the cells. The results obtained showed that the NPs did not significantly affect cell viability. We studied the antioxidant capacity of the NPs by estimating the GSH, TBARs, and Cell Rox content and the enzymatic activity of glutathione peroxidase (GPx). In vitro assays showed that GSH levels, GPx activity and reactive oxygen species (Cell Rox) levels were modified with both concentrations of NPs, while lipoperoxidation (TBARs) decreased when cells exposed to CdCl2 were in contact with the NPs. All these results suggest the ability of NPs to modulate the cell redox state in a dose-dependent manner.