Effect of LncRNA SNHG3/miR-423-5p on IL-1β-Induced Osteoarthritis Chondrocyte Damage

This study was aimed to explore the effect of lncRNA SNHG3 on IL-1β (interleukin-1β)-induced osteoarthritis chondrocyte damage and its possible mechanism. A cell injury model was established by exposing chondrocytes to IL-1β. si-NC, si-SNHG3, miR-NC, miR-423-5p mimics were transfected into chondrocytes and treated with 10 μg/L IL-1β for 24 h. si-SNHG3 and anti-miR-NC, si-SNHG3 and anti-miR-423-5p were co-transfected into chondrocytes and treated with 10 μg/L IL-1β for 24 h. MTT method and flow cytometry were used to detect cell proliferation and apoptosis, respectively. ELISA method was used to detect the levels of IL-6, IL-8 and IL-10. The dual luciferase reporter experiment was used to detect the targeting relationship between SNHG3 and miR-423-5p; Western blot detects the protein expression of Bax and Bcl-2. The expression of SNHG3 in IL-1β-induced chondrocytes was increased (P<0.05), while the expression of miR-423-5p was decreased (P<0.05). After transfection with si-SNHG3 or miR-423-5p mimics, the cell proliferation inhibition rate, apoptosis rate and Bax content were decreased (P<0.05),and the levels of IL-6 and IL-8 were decreased (P<0.05), while IL-10 level and Bcl-2 content were increased (P<0.05). SNHG3 could target miR-423-5p. Anti-miR-423-5p reversed the effects of si-SNHG3 on cells including increased growth, reduced levels of inflammatory factors, decreased IL-10 concentration, and decreased Bcl-2 protein levels (P<0.05). Silencing SNHG3 could negatively regulate the expression of miR-423-5p to promote cell proliferation and inhibit cell apoptosis and inflammation, thereby reducing IL-1β-induced chondrocyte damage.

CSTR: 32200.14.cjcb.2023.09.0003