Fabrication and characterization of ConA-conjugated curcumin-loaded solid lipid nanoparticles for theranostic applications in lung cancer treatment.

The main issues with current and traditional cancer therapy delivery systems include a lack of selectivity towards tumors, causing harm to healthy cells, low efficiency in loading drugs, and the inability to visually track the drug's localization after administration. These limitations negatively impact the effectiveness of therapy and result in increased treatment costs. Furthermore, conventional cancer therapies typically target tumor cells through a single mechanism, which eventually leads to the emergence of drug resistance. Concanavalin A, a plant lectin derived from jack beans, has the ability to recognise cells and can be used as an efficient targeting agent in cancer therapy. In the current study, the effectiveness of solid lipid nanoparticles (SLNs) loaded with curcumin (CU) and conjugated with ConA has been examined in the fight against A549 human lung cancer cells, with a focus on their anticancer properties. This novel strategy allows for targeted delivery, sustained release, and specific recognition of cancer cells. To verify the successful bonding of ConA to SLNs, we conducted a comparison of the FTIR spectra between the synthesized Cur-SLNs and ConA-SLNs and their respective precursors. Additionally, we employed various techniques, such as XRD (X-ray diffraction), DSC (differential scanning calorimetry), TGA (thermogravimetric analysis), SEM (scanning electron microscopy), particle size analysis, and other methods, to examine the surface morphology and viability of SLNs. The present study of drug release revealed a sustained release pattern from the ConA-SLNs. The utilization of targeted nanoparticles resulted in a notable increase in the anticancer effectiveness of curcumin, as demonstrated using an anti-proliferation assay. The positive findings from this research indicate the potential of directing nanomedicines towards carbohydrate structures that are overexpressed through lectin (ConA)-mediated delivery in the treatment of lung cancer.