OBJECTIVE: Two-dimensional difference gel electrophoresis and mass spectrum were used to study the anti-atherosclerosis mechanism of curcumin. METHOD: The proteins from RAW264.7 cell and RAW264.7 cell treated with 25 micromol x L(-1) curcumin were labeled with Cy3 or Cy5 randomly. Each Cy3-labeled sample and Cy5-labeled sample was mixed on the same 2-D gel along with a Cy2-labeled mixture of all samples as an internal standard and run on the same gel. The gels were scanned under different wave-length light after electrophoresis. All images were analyzed by DeCyder 6.5 software, and the different proteins were identified by mass spectrum. RESULT: The expression of ATP synthesis H+ transporting, MHC class II, non-muscle myosin alkali light chain and cytochrome b5 increased in the RAW264.7 cell treated with 25 micromol x L(-1) curcumin, while the expression of phosphodiesterase 4D, elF-3, Hnrpf protein, vimentin, nucleophosminl and Ranbp 1 decreased. CONCLUSION: The anti-atherosclerosis mechanism of curcumin is the result of enhancement of the cell inflammation, antioxidant activity and inhibition of cholesterol transport, reduce of the accumulation of intracellular cholesterol and other factors. In addition, curcumin also had the effect of anti-tumor through regulated tumor cell differentiation and apoptosis.
OBJECTIVE: Two-dimensional difference gel electrophoresis and mass spectrum were used to study the anti-atherosclerosis mechanism of curcumin. METHOD: The proteins from RAW264.7 cell and RAW264.7 cell treated with 25 micromol x L(-1) curcumin were labeled with Cy3 or Cy5 randomly. Each Cy3-labeled sample and Cy5-labeled sample was mixed on the same 2-D gel along with a Cy2-labeled mixture of all samples as an internal standard and run on the same gel. The gels were scanned under different wave-length light after electrophoresis. All images were analyzed by DeCyder 6.5 software, and the different proteins were identified by mass spectrum. RESULT: The expression of ATP synthesis H+ transporting, MHC class II, non-muscle myosin alkali light chain and cytochrome b5 increased in the RAW264.7 cell treated with 25 micromol x L(-1) curcumin, while the expression of phosphodiesterase 4D, elF-3, Hnrpf protein, vimentin, nucleophosminl and Ranbp 1 decreased. CONCLUSION: The anti-atherosclerosis mechanism of curcumin is the result of enhancement of the cell inflammation, antioxidant activity and inhibition of cholesterol transport, reduce of the accumulation of intracellular cholesterol and other factors. In addition, curcumin also had the effect of anti-tumor through regulated tumor cell differentiation and apoptosis.