Curcumin Protected Articular Chondrocyte Injury by Activating TGF-β 1/Smad2 Pathway
Objective To study the effects of curcumin on regulating transforming growth factor-β1(TGF-β1)/signal transduction protein Smad pathway in articular cartilage,and its effects on chondrocyte proliferation,apoptosis,extracellular matrix(ECM)synthesis and degradation.Methods The cells were divided into five groups:control group,model group,curcumin group,inhibitor group,and curcumin+inhibitor group.Cell activity was detected with cell counting kit-8(CCK-8).Flow cytometry was used to detect apoptosis.Western Blot was used to detect expressions of B-cell lymphoma 2 protein(Bcl-2),Bcl-2 associated X protein(Bax),TGF-β1,Smad2,phosphorylated Smad2(p-Smad2),matrix metalloproteinase-13(MMP-13),type Ⅱ collagen(COL2α1)in cells.qRT-PCR was used to detect the mRNA expressions of MMP-13 and COL2α1.Results The optimal dose of curcumin for IL-1β-induced osteoarthritis cell model was 10 μmol/L.Compared with control group,the proliferation ability of cells in model group decreased(P<0.05),the apoptosis rate increased(P<0.05),protein expression levels of Bcl-2,TGF-β1,and p-Smad2 were all down-regulated(P<0.05),mRNA and protein expressions of COL2α1 were down-regulated(P<0.01),Bax protein,MMP-13 mRNAand protein expressions were all up-regulated(P<0.05)Compared with model group,cell proliferation increased(P<0.05),apoptosis rate decreased(P<0.05),protein expression levels of Bcl-2,TGF-β 1,and Smad2 were up-regulated(P<0.05),mRNA and protein expressions of COL2α1 were up-regulated(P<0.05),Bax protein,MMP-13 mRNA and protein expressions were all down-regulated(P<0.05)in curcumin group.TGF-β1 inhibitor aggravated the injury of model cells.Compared with TGF-β inhibitor group,an opposite trend showed in curcumin+inhibitor group.Conclusion Curcumin ameliorated IL-1β-induced articular chondrocyte injury,attenuated apoptosis,and thus further inhibited ECM degradation,which was possibly associated by activating TGF-β1/Smad2 pathway.
osteoarthritiscurcuminTGF-β1/Smad2 pathwayapoptosisdegradation of extracellular matrix