Considering interference with cellular adhesion, curcumin and CurcuEmulsomes ca

Upon dissolution in an organic solvent, curcumin ab sorbs light in the visible wavelength MAPK 阻害剤 range, Turmeric contains three major analogues: curcumin, demethoxycur cumin, and bisdemethoxycurcumin and recently identified cyclocurcumin in less signifi cant amounts, Commercially available curcumin mix ture contains approximately 77% curcumin, 17% DMC and 3% BDMC as major components, Although all three are highly active, curcumin is more efficient than DMC and BDMC on various cell models, Con trary to these findings, studies on preclinical models of carcinogenesis have demonstrated that commercial grade curcumin turmeric as a mixture has the same inhibitory effect as pure curcumin, Pharmacologically regarded as safe, curcumin is non toxic, even at relatively high doses such as 8 g per day, As demonstrated recently, tumor cells are more sensitive to the cytotoxic activity of curcumin than nor mal cells, In line with another study, the cellular up take of curcumin was found to be significantly higher in tumor cells compared to normal cells, which was attrib uted to the differentiated membrane structure, protein composition and bigger size, The lower uptake rate may explain the low toxicity of curcumin for healthy cells.<br><br> The wide spectrum of pharmacological properties of curcumin is attributed to its numerous effects MK-1775 wee1 阻害剤 on several targets including transcription factors, growth regula tors, adhesion molecules, apoptotic genes, angiogenesis regulators, and cellular signaling molecules, Curcu min exerts anti cancer activity mainly through blocking cell cycle progression and triggering tumor cell apoptosis, All three stages of carcinogenesis including initi ation, promotion and progression are suppressed by cur cumin, This is probably due to inhibition of the nuclear factor κB, which plays a central role in regulat ing the expression of various genes involved in cell sur vival, apoptosis, carcinogenesis and inflammation.<br><br><br><br> This efficacy makes curcumin to a potential therapeutic target, Furthermore, curcumin affects various cell cycle proteins and checkpoints involving downregulation of some of the cyclins and cyclin dependent kinases, upregulation of cdk inhibitors, and inhibition of DNA syn thesis, However, the physiological response triggered by cms-275 209783-80-2 urcumin depends on the cell type, the concentration of curcumin and the time of treatment, For instance, curcumin treatment was reported to ar rest cell growth at phase and induce apoptosis in human hepatoma cell line HepG2, whereas G0 G1 as well as G1 S phase arrests were reported for various other cell lines, Clinical use of curcumin remains very limited due to its extremely poor water solubility, and low bioavailability following oral administration, Even when 10 12 g ml of curcumin was administered orally in humans, curcumin levels in serum remained approximately at 50 ng ml, Several studies demon strated that 10 50 curcumin in duces cell death primarily through apoptosis, However, the important question to be addressed is how to bring curcumin at these micromolar concentrations to the site of tumors while curcumin possesses such a low bioavailability.<br><br> Addressing this problem, targeted and triggered drug delivery systems accompanied by nanoparticle technology have emerged as prominent so lutions, Likewise, this study introduces emulsomes as a promising nanocarrier system suitable for the deliv ery of curcumin. Emulsomes are biocompatible vesicular systems com prising of a solid fat core surrounded by phospholipid multi layers, Due to the solid core, emul somes can entrap higher amounts of lipophilic drug compounds with a prolonged release time compared to emulsion formulations possessing a liquid core, Composed of fat and lipids, emulsomes are biocompat ible.