Accord ingly, CurcuEmulsomes accumulate inside the cell before any sufficient release of the load could occur. This finding may explain why CurcuEmulsomes caused cytotoxicity only after 24 hours. Cell cycle analysis demonstrated NSC 683864 that CurcuEmul somes cause a prolonged induction of G2 M cell cycle arrest where the peak of G2 M phase rose steadily from 6 to 48 hours. In the contrary, free curcumin results in a sharp increase after 24 hours which declined Inhibitors,Modulators,Libraries after 48 hours. These findings, in line with cytotoxicity data, corroborate the slow and sustained release of curcumin from CurcuEmulsomes into the cells. Cell cycle analyses were only performed for 48 hours be cause the low viability profiles of treated HepG2 cells did not allow longer investigations.

How ever, speculatively, a further increase in G2 M phase arrest might be predicted due to the slow release pro file of emulsomes. Conclusions Introducing a new nanocarrier system for curcumin, the present study illustrates the particular characteristics of CurcuEmulsomes Inhibitors,Modulators,Libraries and investigates Inhibitors,Modulators,Libraries the delivery of curcu min into the cell in vitro, where HepG2 cell line is used as a model. In summary it may be concluded that i cur cumin can be incorporated into the emulsomes, ii the incorporation enhances the poor water solubility of this bioactive polyphenol, iii upon incorporation, biological activity as well as fluorescence integrity of curcumin is preserved, iv delivered within a solid lipid core, curcu min is gradually released into the cell, thereby resulting in prolonged cytotoxicity and cell cycle arrest on HepG2, v due to its prolonged activity, the incorporated curcu min acts, on long terms, as efficient as free curcumin dissolved in organic solvent.

Consequently, enabling cur cumin to reach its effective concentrations Inhibitors,Modulators,Libraries Inhibitors,Modulators,Libraries inside the cell, the presented approach may allow therapeutic ap plications of curcumin, and with future perspectives, provide an alternative platform for the delivery of hydro phobic bioactive agents whose medical use is otherwise limited. Methods Materials Curcumin, glyceryl tripalmitate, 1,2 dipalmitoyl rac glycero 3 phosphatidylcholine, glutaraldehyde solution, glycerol and Dulbeccos Phosphate Buffered Saline were purchased from Sigma Aldrich GmbH, Germany. Hexa decylamine, uranyl acetate dehydrate, methanol and chloroform were obtained from Fluka Chemika, Germany. Choles terol was purchased from Avanti Polar Lipids, US. Dimethyl sulfoxide was purchased from Riedel de Ha?n. 4. 6 Diamidino 2 phenylindole dihydrochloride was purchased from AppliChem GmbH, Germany. All chemicals were used as purchased without any further purification. Cell line HepG2 screening library was obtained from American Type Culture Collection.