| ObjectiveTo investigate the effect of LncRNA FGD5-AS1 targeting miR-103a-3p on IL-1β-induced articular chondrocyte injury and apoptosis and its molecular mechanism. Methods Rat articular chondrocytes were cultured in vitro and divided into NC group and IL-1β group (IL-1β 10 ng / mL). The expression levels of FGD5-AS1 and miR-103a-3p in cells were detected by qRT-PCR. PcDNA-FGD5-AS1, miR-103a-3p mimics were transfected into chondrocytes respectively, and then treated with IL-1β for 48 h. ELISA was used to detect the levels of IL-6, TNF-α and IL-8. Flow cytometry was used to detect the apoptotic rate. The dual luciferase report experiment verified the targeting relationship between FGD5-AS1 and miR-103a-3p. Western blot was used to detect the expression levels of Bax, Cyt C, Cleaved Caspase-3, p-NF-κB p65, and p-IκBα protein . Results Compared with the NC group, the expression level of FGD5-AS1 in chondrocytes in the IL-1β group was significantly reduced (P<0.05), and the expression levels of miR-103a-3p, Bax, Cyt C, and Cleaved Caspase-3 were significantly increased (P <0.05), the levels of IL-6, TNF-α and IL-8 were significantly increased (P <0.05), and the apoptosis rate was significantly increased (P<0.05). FGD5-AS1 overexpression could significantly reduce the levels of IL-6, TNF-α, IL-8, p-NF-κB p65, and p-IκBα (P <0.05), reduced the rate of apoptosis (P<0.05), and inhibited Bax, Cyt C, and Cleaved Caspase-3 expression (P<0.05). The double luciferase reporting experiment confirmed that FGD5-AS1 targets miR-103a-3p and could negatively regulate the expression of miR-103a-3p (P<0.05). Overexpression of miR-103a-3p could significantly reverse the inhibitory effect of FGD5-AS1 overexpression on apoptosis and inflammatory response (P<0.05). Conclusion LncRNA FGD5-AS1 could negatively regulate the expression of miR-103a-3p, thereby inhibiting IL-1β-induced articular chondrocyte inflammation and apoptosis, and its mechanism may be related to the inhibition of NF-κB signaling pathway activation. |