Abstract: Objective To explore the effect of long non-coding RNA ( lncRNA) X inactivespecific transcript ( XIST) on interleukin-1β ( IL-1β ) -induced chondrocyte apoptosis and itsmechanism. Methods The targeting relationship between XIST and miR-124 was predicted bybioinformatics and verified by dual luciferase reporter gene assay. Ten experimental groups were set as follows: normal group, IL-1β group, si-NC group, si-XIST group, miR-124-NC group, miR-124 mimics group, si-NC + inhibitor-NC group, si-XIST + inhibitor-NC group, si-NC + miR-124inhibitor group, si-XIST + miR-124 inhibitor group. qRT-PCR was used to detect the expression levels of XIST and miR-124 in cells. Western blotting was used to detect the expression level of nuclearfactor kappa B P65 ( NF-κB P65 ) protein. Flow cytometry was used to detect cell apoptosis. Results There was a targeting relationship between lncRNA XIST and miR-124. The expressionlevels of lncRNA XIST and NF-κB P65 protein and the apoptosis rate in the IL-1β-induced chondrocytes were increased, while the expression level of miR-124 was decreased when compared withthose in the normal group (P < 0. 05). The expression level of NF-κB P65 protein and the apoptosisrate in the si-XIST group and the miR-124 mimics group were reduced when compared with those inthe IL-1β group (P < 0. 05). The expression level of NF-κB P65 protein and the cell apoptosis rate in the si-XIST + inhibitor-NC group were reduced when compared with those in the si-NC + inhibitorNC group. The expression level of NF-κB P65 protein and the apoptosis rate in the si-XIST + miR-124 inhibitor group were decreased when compared with those in the si-NC + miR-124 inhibitorgroup, ( P < 0. 05). Conclusion Down-regulation of lncRNA XIST can target and regulate themiR-124 / NF-κB axis, thereby alleviating the apoptosis of chondrocytes induced by IL-1β.

Key words: long non-coding RNA XIST, miR-124, NF-κB, chondrocytes, apoptosis