MiR-30a-3p Promote Proliferation And Inhibit Apoptosis Of Chondrocytes Via Inhibit Wnt2 In Osteoarthritis

Objective:The purpose of this study was to confirm the abnormal expression of mi R-30a-3p and Wnt2 in chondrocytes of OA patients,and to explore the correlation between the effect of mi R-30a-3p on proliferation and apoptosis of chondrocytes and OA disease by inhibiting Wnt2 and affecting the activation of Wnt/β-catenin signaling pathway.Methods:1.In vitro culture of knee chondrocytes from OA patients.2.The expression levels of mi R-30a-3p and Wnt2 in OA chondrocytes were detected by QRT-PCR.Western blotting was used to measure the expression of Wnt2,IL-6 and type II collagen.3.After OA chondrocytes were transfected with mi R-30a-3p overexpression and inhibitor,cc K-8 assay and flow cytometry were used to observe the effects of mi R-30a-3p overexpression and inhibition on chondrocyte proliferation and apoptosis,and the changes of Wnt2,IL-6 and type II collagen were measured.4.Plasmid transfection and double luciferase reporting assay were used to verify the relationship between mi R-30a-3p and Wnt2.Results:This study confirmed that the expression level of mi R-30a-3p in OA chondrocytes was lower than that in normal chondrocytes(P < 0.01),while the expression level of Wnt2 was increased(P < 0.001).The experimental results showed that mi R-30a-3p could directly target Wnt2 to affect the proliferation and apoptosis of OA chondrocytes,and mi R-30a-3p inhibited the expression of Wnt2 in the mutual regulation relationship(P < 0.05):(1)Overexpression of mi R-30a-3p and CCK-8showed significantly increased proliferation activity of chondrocytes(P < 0.001)and decreased expression of IL-6(P < 0.05).(2)Inhibition of mi R-30a-3p increased the late apoptosis rate of OA chondrocytes(P < 0.001)and inflammatory markers(P <0.001).Conclusions:1.Compared with normal chondrocytes,the expression of mi R-30a-3p was down-regulated in OA chondrocytes,while the expression of Wnt2 was increased.2.Overexpression of mi R-30a-3p in chondrocytes increased the proliferation activity of chondrocytes and reduced the apoptosis rate of chondrocytes and the generation of inflammatory markers.3.The decrease of mi R-30a-3p in chondrocytes weakened the proliferation activity of chondrocytes and increased the apoptosis rate of chondrocytes and the expression of inflammatory markers.4.mi R-30a-3p in chondrocytes can affect the activation of Wnt/β-catenin signaling pathway by inhibiting the expression of Wnt2,regulate the proliferation and apoptosis of chondrocytes,and may eventually participate in the disease process of OA.