Department of Orthopedics, The Affiliated Taizhou People's Hospital of Nantong University, Taizhou, Jiangsu 225300, P.R. China.
Department of Orthopedics, Nanjing Central Hospital, Nanjing, Jiangsu 210018, P.R. China.
Mol Med Rep. 2019 Oct;20(4):3867-3873. doi: 10.3892/mmr.2019.10639. Epub 2019 Sep 2.
Osteoarthritis (OA) is one of the most prevalent types of chronic joint diseases. Chondrocytes survival is closely associated with the destruction of joints in patients with OA. Long noncoding RNAs (lncRNAs) serve a critical role in OA. However, to the best of our knowledge, the role of lncRNAs NR024118 in OA has not been examined. In the present study, the expression levels of NR024118 in lipopolysaccharide (LPS)‑induced chondrocytes was measured using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and the apoptosis levels of cells was determined using flow cytometry. The levels of scavenged reactive oxygen species and expression levels of the antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), and heme oxygenase‑1 (HO‑1) were measured using specialized detection kits. The expression of interleukin (IL)‑1β, IL‑6 and IL‑18 were measured using ELISA. Expression of the cell apoptosis markers Bcl‑2, Bax, Bcl‑2‑like protein 11, NF‑κB, phosphorylated (p)‑NF‑κB inhibitor β (IκBβ), IκBβ, p‑transcription factor p65 (p65) and p65, and nuclear factor erythroid‑2 related factor 2 (Nrf2) signaling pathways‑associated proteins, Nrf2, HO‑1 and quinone oxidoreductase‑1 were detected by western blot analysis and RT‑qPCR. The results indicated that in ATDC5 cells, apoptosis, oxidative stress and inflammation were significantly increased and the expression level of NR024118 was significantly decreased by LPS‑mediated induction. NR024118 overexpression significantly reversed the effects of LPS treatment in the ATDC5 cell line. In addition, the overexpression of NR024118 decreased NF‑κB expression levels and activated the Nrf2 signaling pathways in LPS‑induced ATDC5 cells. The present study demonstrated that NR024118 attenuated the effects of LPS‑induction on ATDC5 cells. These results suggest that NR024118 may be a potential target for diagnosis and treatment of OA.
骨关节炎（OA）是最常见的慢性关节疾病之一。软骨细胞的存活与 OA 患者关节的破坏密切相关。长链非编码 RNA（lncRNA）在 OA 中发挥着关键作用。然而，据我们所知，lncRNA NR024118 在 OA 中的作用尚未被研究过。在本研究中，通过逆转录-定量聚合酶链反应（RT-qPCR）测量脂多糖（LPS）诱导的软骨细胞中 NR024118 的表达水平，并通过流式细胞术测定细胞凋亡水平。使用专门的检测试剂盒测量清除活性氧的水平和抗氧化酶的表达水平，包括超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和血红素加氧酶-1（HO-1）。通过 ELISA 测量白细胞介素（IL）-1β、IL-6 和 IL-18 的表达水平。通过 Western blot 分析和 RT-qPCR 检测细胞凋亡标志物 Bcl-2、Bax、Bcl-2 样蛋白 11、核因子-κB（NF-κB）、磷酸化（p）-NF-κB 抑制剂β（IκBβ）、IκBβ、p-转录因子 p65（p65）和 p65 以及核因子红细胞 2 相关因子 2（Nrf2）信号通路相关蛋白，Nrf2、HO-1 和醌氧化还原酶 1 的表达。结果表明，在 ATDC5 细胞中，LPS 介导的诱导作用显著增加了细胞凋亡、氧化应激和炎症反应，NR024118 的表达水平显著降低。NR024118 的过表达显著逆转了 LPS 处理对 ATDC5 细胞系的作用。此外，NR024118 的过表达降低了 LPS 诱导的 ATDC5 细胞中 NF-κB 的表达水平，并激活了 Nrf2 信号通路。本研究表明，NR024118 减轻了 LPS 诱导对 ATDC5 细胞的影响。这些结果表明，NR024118 可能是 OA 诊断和治疗的潜在靶点。
