Osteoarthritis (OA), a type of joint diseases, could result in breakdown of joint cartilage and underlying bone. Accumulatingevidences suggested that long non-coding RNAs play important roles in OA progression. However, the underlyingmechanism of H19 in OA is still not fully explored. The expression levels of H19 and miR-106a-5p in OA samples frompatients or cultured chondrocytes were examined by quantitative real time polymerase chain reaction. Cell proliferation andapoptosis were analysed by MTT assay and flow cytometry, respectively. Western blotting was employed to detect theexpression levels of PCNA, CyclinD1, Caspase 3 and Cleaved Caspase 3. StarBase database, luciferase assay and RNAimmunoprecipitation were introduced to confirm the relationship between H19 and miR-106a-5p. The correlation of H19and miR-106a-5p was analysed by Spearman rank analysis. H19 expression was upregulated, while miR-106a-5p level wasdownregulated in OA samples and IL-1beta-treated chondrocytes. H19 overexpression inhibited the proliferation and inducedapoptosis in IL-1beta-treated chondrocytes, while H19 knockdown induced the opposite effect. Luciferase and RIP assaydemonstrated that miR-106a-5p was a direct target of H19. miR-106a-5p overexpression led to proliferation promotion andapoptosis inhibition in chondrocytes treated by IL-1beta and it reversed the effect of H19 addition. We conclude that H19could regulate proliferation and apoptosis of chondrocytes treated by IL-1beta in OA via sponging miR-106a-5p.