Long non-coding RNA MIR155HG regulates IL-1β-induced inflammatory injury in osteoarthritis chondrocytes

CHEN Xiaochao; MA Tiancheng; ZOU Jiwei

doi:10.3969/j.issn.1002-7386.2024.07.002

Abstract：Objective To explore the regulatory effect of long non-coding RNA MIR155 host gene(MIR155HG)on interleukin 1β(IL-1β)-induced inflammatory injury of osteoarthritis chondrocytes and the underlying mechanism.Methods The in vitro model of osteoarthritis was established by stimulating chondrocytes with IL-1β at 10ng/mL for 24h.The chondrocytes were treated with blank control,induced with IL-1β,transfected with NC siRNA(si-NC)for 48h and induced with IL-1β,or transfected with MIR155HG siRNA(si-MIR155HG)for 48 h and induced with IL-1β.The expression level of MIR155HG was examined using the real-time quantitative reverse transcription polymerase chain reaction(RT-qPCR).The survival rate of chondrocytes was detected using the Calcein AM Cell Viability Assay Kit.The apoptosis of chondrocytes was evaluated using the terminal deoxynucleotidyl transferase dUTP nick end labeling(TUNEL)Apoptosis Assay Kit.The protein levels of Bax,Bcl-2,matrix metallopeptidase-13(MMP-13),collagen type Ⅱ alpha 1(COL2A1),NLR-family pyrin domain-containing protein 3(NLRP3),ASC,and Caspase-1 were measured by Western blot.The concentrations of interleukin 6(IL-6),tumor necrosis factor-alpha(TNF-α),and interleukin 18(IL-18)were quantified by the enzyme linked immunosorbent assay(ELISA)kits.Results Compared with that of blank control,MIR155HG was significantly upregulated in IL-1β-induced chondrocytes(P<0.01).It was significantly downregulated in IL-1β-induced chondrocytes transfected with si-MIR155HG than those transfected with si-NC(P<0.01).Compared with that of blank control,IL-1β-induced chondrocytes and those transfected with si-NC presented significantly lower cell viability,and significantly higher apoptotic rate,degradation of extracellular matrix,relative levels of IL-6,TNF-α and IL-18 and protein levels of NLRP3,ASC and caspase-1(all P<0.01).Compared with those induced with IL-1β with either the transfection of si-NC or not,IL-1β-induced chondrocytes transfected with si-MIR155HG presented significantly higher cell viability,and significantly lower apoptotic rate,degradation of extracellular matrix,relative levels of IL-6,TNF-α and IL-18 and protein levels of NLRP3,ASC and caspase-1(all P<0.01).Conclusion Silence of lncRNA MIR155HG ameliorates IL-1β-induced inflammatory injury of chondrocytes by inhibiting the activation of NLRP3 inflammasome.