[Effects of long non-coding RNA KLHL7-AS1 on the proliferation and apoptosis of nucleus pulposus cells under the environment of oxidative stress and its mechanism].

<b>Objective:</b> To investigate the effects of long non-coding RNA KLHL7-AS1 (LncRNA KLHL7-AS1) on the proliferation and apoptosis of nucleus pulposus cells under oxidative stress and its mechanisms. <b>Methods:</b> Human nucleus pulposus cells (HUM-iCell-s012) were divided into 4 groups, and unoxidized nucleus pulposus cells were transfected with an empty pcDNA vector (pcDNA-control) to serve as the blank control group. Based on previous studies on oxidative stress-induced nucleus pulposus cell senescence and preliminary experiments, oxidative stress was induced by treating nucleus pulposus cells with 400 μmol/L H₂O₂. Oxidized nucleus pulposus cells were transfected with pcDNA-control, KLHL7-AS1 interfering RNA (siRNA-KLHL7-AS1), or KLHL7-AS1 overexpression plasmid (pcDNA-KLHL7-AS1), forming the model control group (H₂O₂+pcDNA-control), the model silencing group (H₂O₂+siRNA-KLHL7-AS1), and the model overexpression group (H₂O₂+pcDNA-KLHL7-AS1), respectively. Following these treatments, KLHL7-AS1 expression levels, cell proliferation, cell apoptosis were measured and compared among the groups, and the expression levels of B-cell lymphoma 2 (BCL-2) and BCL-2-associated X protein (BAX) in the groups of cells were compared too (<i>n</i>=3). <b>Results:</b> The expression of KLHL7-AS1 in the model control group was significantly higher than that in the blank control group (7.716±0.851 vs 0.996±0.086, <i>P</i><0.001). Furthermore, the expression of KLHL7-AS1 in the model overexpression group was markedly higher than that in the model silencing group (19.592±1.747 vs 4.222±0.039, <i>P</i><0.001). Compared to the blank control group, the model silencing group showed no significant change in cell viability (0.125±0.006 vs 0.127±0.010, <i>P</i>=0.390), an increased apoptosis rate (17.2%±1.7% vs 11.5%±1.0%, <i>P</i><0.05), elevated BCL-2 protein expression (0.897±0.025 vs 0.730±0.026, <i>P</i><0.05), and reduced BAX protein expression (0.250±0.030 vs 0.523±0.015, <i>P</i><0.05). In comparison to the model control group, the model silencing group exhibited increased cell viability (0.125±0.006 vs 0.076±0.008), reduced apoptosis rates (17.2%±1.7% vs 30.7%±2.3%), elevated BCL-2 protein expression (0.730±0.026 vs 0.440±0.036), and decreased BAX protein expression (0.523±0.015 vs 0.723±0.021) (all <i>P</i><0.001). In comparison to the model silencing group, the model overexpression group showed reduced cell viability (0.125±0.006 vs 0.039±0.006), increased apoptosis rates (43.1%±1.9% vs 17.2%±1.7%), decreased BCL-2 protein expression (0.227±0.021 vs 0.730±0.026), and increased BAX protein expression (1.147±0.035 vs 0.523±0.015) (all <i>P</i><0.001). <b>Conclusions:</b> Downregulation of KLHL7-AS1 expression promotes the proliferation of nucleus pulposus cells and inhibits their apoptosis, it may involve the regulation of BCL-2 and BAX protein synthesis, potentially delays the progression of intervertebral disc degeneration.