Conjugation of Dexamethasone to C60 for the Design of an Anti-Inflammatory Nanomedicine with Reduced Cellular Apoptosis

Dexamethasone (DEX) is a well-known anti-inflammatory drug, whose widespread clinical use is nevertheless restricted by its serious side effects. By conjugation of DEX with C-60, we found that this nanomedicine retained the anti-inflammatory activity of DEX while reducing side effects in the animal model. In mouse thymocytes, the CCK-8 assay showed that the cytotoxicity of DEX-C-60 was significantly lower than that of free DEX. Flow cytometric studies revealed that incubation with DEX-C-60 induced much less apoptotic thymocytes. Interestingly, such reduced cytotoxicity and apoptosis were not observed when equal moles of free C-60 and free DEX were coincubated with thymocytes suggesting that the conjugation alters the signal pathway of DEX Indeed, found that the binding of DEX-C-60 and a glucocorticoid receptor (GR) was partially blocked in the thymocytes, which resulted in down-regulation of several apoptosis-related genes. These findings help understand the mechanism of beneficial effects of this new nanomedicine, DEX-C-60, and promote its clinical applications.