The Effect Of Curcumin On Palmitic Acid Induced Inflammation And Fibrosis Pathway In HepG2Cells

Obejective:To investigate the effect of curcumin on palmitic acid induced inflammation and fibrosis pathway in HepG2cells and its possible mechanisms.Methods:In vitro, HepG2cells steatosis model were established by dealed with PA. The change of the number and size of intracellular lipid droplets with PA or PA and curcumin were determined by Oil red O staining.Using Western Blot to detect the protein levels of Toll-like receptors4(TLR4), myeloid differentiation primary response gene88(MyD88) and Nuclear Factor-kappa B(NF-κB) in HepG2cells dealed with PA or PA and different concentrations of curcumin for24hours.Using Westen Blot to detect the protein levels of transforming growth factor β1(TGF-β1), Smad2and Smad3in HepG2cells dealing with PA or PA and different concentrations of curcumin treatment for24hours.Results:Oil red O staining:red fat droplets in HepG2cells were increased by PA, and were attenuated by curcumin (P<0.01v.s PA group); There are no significant difference compared with control group.TLR4protein was detected in HepG2cells, PA treatment for24h significantly increased its levels (P<0.01v.s control group).Compared with PA group, protein levels of TLR4, MyD88and NF-κB in different concentrations curcumin groups were significantly decreased (P<0.01for all v.s PA group), high curcumin concentration group even lower than control group (P<0.01-0.05).Compared with PA group, protein levels of TGF-β1, Smad2and Smad3in different concentrations curcumin groups were significantly decreased (P<0.01for all v.s PA group).Compared with the control group, high concentration curcumin group also descended.Conclusion:Curcumin alleviated the fatty deposits induced by PA in HepG2cells. Curcumin might improve liver inflammation in the early state by inhibiting the TLR4/NF-κB signal transduction pathway, and this way is MyD88dependent.Curcumin could inhibit the TGF-β1/Smad pathway, might be conducive to prevent liver fibrosis.