[Objective]To study the effect of curcumin on the cholesterol metabolism of nonalcoholic fatty liver disease(NAFLD) cells model induced in vitro and its potential mechanism. [ Methods]The cellmodel of nonalcoholic fatty liver disease(NAFLD) was established by oleic acid and treated with curcumin. The method of oil red O staining was used to observe accumulation of intracellular lipid while the intracellular content of TG, FC and TC was detected by enzymatic method. Meanwhile, the mRNA levels of SR-BΙand HMGCR were detected with qPCR.[ Results] The NAFLD cellmodel was successful y established by culturing with 30 μg·mL-1 oleic acid. After curcumin intervention, TG, FC and intracellular lipid accumulation levels were significantly reduced in NAFLD cellmodel. Meanwhile, curcumin can reduce HMGCR mRNA expression and raise SR-BΙ mRNA expression. [Conclusion] Curcumin can decrease FC level in NAFLD cellmodel and the mechanism might be related with its capacity of restraining endogenous cholesterol biosynthesis and promoting foreign cholesterol transfer into the liver cells for metabolism.

OBJECTIVETwo-dimensional difference gel electrophoresis and mass spectrum were used to study the anti-atherosclerosis mechanism of curcumin.

METHODThe 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.

RESULTThe 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.

CONCLUSIONThe 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.

Animals ; Atherosclerosis ; metabolism ; Cell Line ; Curcumin ; pharmacology ; Electrophoresis, Gel, Two-Dimensional ; methods ; Gene Expression ; drug effects ; Major Histocompatibility Complex ; physiology ; Mass Spectrometry ; Mice ; Proteomics ; methods ; Reverse Transcriptase Polymerase Chain Reaction