To study and analyze the mechanism of icariin on TDP-43 mediated chondrocytic lesions in osteoarthritis，so as to provide a reference for effective treatment of chondrocystic lesions in osteoarthritis.Methods：TDP43 lentivirus was transfected into human chondrocytes，and intervened by icariin with different concentrations.Fluorescence quantitative PCR was used to detect the expression of TDP-43 gene in different groups of human chondrocytes.Flow cytometry was used to detect the apoptosis of human chondrocytes transfected with TDP43 lentivirus before and after the addition of icariin.Three sets of target genes in human cartilage cells TDP43 and collagen expression in alpha 1 Ⅰ type，the cell apoptosis of TDP43 lentivirus transfection human cartilage cells before and after adding icariin，cartilage cell count after cultivation by adding different concentration of icariin were compared respectively.Results：TDP43 gene expression level in human chondrocytes transfected with TDP43(16.02±1.45)was higher than that in normal human chondrocytes and human chondrocytes transfected with lentivirus(1.86±0.13)and(1.88±0.12)，with statistically significant differences(all P<0.05).The comparison of Ⅰ type collagen and three groups of alpha 1 gene expression levels were not obvious(P>0.05).The apoptosis rate of human chondrocytes transfected with TDP43 lentivirus after adding different concentrations of icariin was lower than before adding icariin，with statistically significant differences(all P<0.05).The chondrocytes cultured with high concentration of icariin after 3 d，6 d and 12 d cultivation were higher than the medium concentration，while the chondrocytes cultured with medium concentration of icariin were higher than the low concentration.And one-way analysis of variance showed that the difference between the groups was statistically significant(all P<0.05).Conclusion：TDP-43 may play a negative regulatory role in osteoarthritis chondrocytic lesions，while icariin can improve the above process and further improve the TDP-43 mediated chondrocytic lesions in osteoarthritis.