Suppr超能文献

软骨寡聚基质蛋白聚糖诱导的白细胞介素-1β和肿瘤坏死因子-α对退变髓核细胞的作用。

Effects of kartogenin on the attenuated nucleus pulposus cell degeneration of intervertebral discs induced by interleukin-1β and tumor necrosis factor-α.

机构信息

Department of Orthopaedics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210000, P.R. China.

出版信息

Int J Mol Med. 2018 Feb;41(2):749-756. doi: 10.3892/ijmm.2017.3283. Epub 2017 Nov 24.

Abstract

Cytokines are the main cause of intervertebral disc degeneration. Kartogenin (KGN) is found to protect chondrocytes from cytokines. To explore whether KGN can slow down the degeneration on intervertebral discs following exposure to interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF‑α), the expression of type II collagen (Col II) and aggrecan were detected by immunofluorescence, immunohistochemistry and tissue staining. An in vitro model of disc degeneration using human nucleus pulposus cells (hNPCs) and ex vivo culture of mouse intervertebral discs organs under the actions of inflammatory cytokines were used, and the expression of Col II and aggrecan in hNPCs were detected by semi-quantitative western blot analysis, and the mRNA expression of the genes than encode Col II and aggrecan were detected by reverse transcription‑quantitative polymerase chain reaction (RT-qPCR). The results indicated that the expression of Col II and aggrecan was reduced in the degeneration models. However, the protein expressions of Col II and aggrecan were significantly elevated in hNPCs and the mouse intervertebral discs following addition of KGN. RT-qPCR results revealed that the mRNA expression of Col II and aggrecan was increased in hNPCs and mouse intervertebral discs following treatment with KGN. Thus, KGN effectively increased the expression of Col II and aggrecan in hNPCs and slowed the degeneration of intervertebral discs stimulated by IL-1β and TNF-α.

摘要

细胞因子是椎间盘退变的主要原因。现已发现 Kartogenin(KGN)可保护软骨细胞免受细胞因子的侵害。为了探讨 KGN 是否能减缓白细胞介素 1β(IL-1β)和肿瘤坏死因子-α(TNF-α)作用下的椎间盘退变,通过免疫荧光、免疫组化和组织染色检测了 II 型胶原(Col II)和聚集蛋白聚糖的表达。使用人髓核细胞(hNPCs)体外椎间盘退变模型和炎性细胞因子作用下的小鼠椎间盘器官的体外培养,通过半定量 Western blot 分析检测 hNPCs 中 Col II 和聚集蛋白聚糖的表达,并通过逆转录-定量聚合酶链反应(RT-qPCR)检测编码 Col II 和聚集蛋白聚糖的基因的 mRNA 表达。结果表明,退变模型中 Col II 和聚集蛋白聚糖的表达减少。然而,在加入 KGN 后,hNPCs 和小鼠椎间盘的 Col II 和聚集蛋白聚糖的蛋白表达明显升高。RT-qPCR 结果显示,KGN 处理后 hNPCs 和小鼠椎间盘的 Col II 和聚集蛋白聚糖的 mRNA 表达增加。因此,KGN 能有效增加 hNPCs 中 Col II 和聚集蛋白聚糖的表达,减缓 IL-1β 和 TNF-α 刺激的椎间盘退变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc60/5752177/6fed13dbcfbd/IJMM-41-02-0749-g00.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验