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首页> 外文期刊>Cellular Physiology and Biochemistry >N-Cadherin Attenuates High Glucose-Induced Nucleus Pulposus Cell Senescence Through Regulation of the ROS/NF-κB Pathway
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N-Cadherin Attenuates High Glucose-Induced Nucleus Pulposus Cell Senescence Through Regulation of the ROS/NF-κB Pathway

机译：N-钙黏着蛋白通过调节ROS /NF-κB途径减弱高糖诱导的髓核细胞衰老

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Background/Aims Diabetes mellitus (DM) is a potential etiology of disc degeneration. N-cadherin (N-CDH) helps maintain the cell viability, cell phenotype and matrix biosynthesis of nucleus pulposus (NP) cells. Here, we mainly aimed to investigate whether N-CDH can attenuate high glucose-induced NP cell senescence and its potential mechanism. Methods Rat NP cells were cultured in a base culture medium and base culture medium with a 0.2 M glucose concentration. Recombinant lentiviral vectors were used to enhance N-CDH expression in NP cells. Senescence-associated β-galactosidase (SA-β-Gal) activity was measured by SA-β-Gal staining. NP cell proliferation was evaluated by CCK-8 assay. Telomerase activity and intracellular reactive oxygen species (ROS) content were tested by specific chemical kits according to the manufacturer’s instructions. G0/G1 cell cycle arrest was evaluated by flow cytometry. Real-time PCR and Western blotting were used to analyze mRNA and protein expressions of senescence markers (p16 and p53) and matrix macromolecules (aggrecan and collagen II). Additionally, p-NF-κB expression was also analyzed by Western blotting to evaluate NF-κB pathway activity. Results High glucose significantly decreased N-CDH expression, increased ROS generation and NF-κB pathway activity, and promoted NP cell senescence, which was reflected in the increase in SA-β-Gal activity and senescence marker (p16 and p53) expression, compared to the control group. High glucose decreased telomerase activity and cell proliferation potency. However, N-CDH overexpression partially attenuated NP cell senescence, decreased ROS content and inhibited the activation of the NF-κB pathway under the high glucose condition. Conclusion High glucose decreases N-CDH expression and promotes NP cell senescence. N-CDH overexpression can attenuate high glucose-induced NP cell senescence through the regulation of the ROS/ NF-κB pathway. This study suggests that N-CDH is a potential therapeutic target to slow DM-mediated disc NP degeneration.
机译：背景/目的糖尿病（DM）是椎间盘退变的潜在病因。 N-钙粘蛋白（N-CDH）有助于维持髓核（NP）细胞的细胞活力，细胞表型和基质生物合成。在这里，我们主要旨在研究N-CDH是否可以减弱高糖诱导的NP细胞衰老及其潜在机制。方法在基础培养基和0.2 M葡萄糖浓度的基础培养基中培养大鼠NP细胞。重组慢病毒载体用于增强NP细胞中N-CDH的表达。通过SA-β-Gal染色测量衰老相关的β-半乳糖苷酶（SA-β-Gal）活性。 NP细胞增殖通过CCK-8分析评估。端粒酶活性和细胞内活性氧（ROS）含量已根据制造商的说明通过特定的化学试剂盒进行了测​​试。通过流式细胞仪评估G0 / G1细胞周期停滞。实时荧光定量PCR和Western印迹分析衰老标志物（p16和p53）和基质大分子（aggrecan和胶原蛋白II）的mRNA和蛋白表达。另外，还通过蛋白质印迹分析了p-NF-κB的表达以评估NF-κB途径的活性。结果高糖显着降低N-CDH表达，增加ROS生成和NF-κB通路活性并促进NP细胞衰老，这反映在SA-β-Gal活性和衰老标志物（p16和p53）表达的增加上到对照组。高葡萄糖会降低端粒酶活性和细胞增殖能力。然而，在高葡萄糖条件下，N-CDH的过表达部分减弱了NP细胞的衰老，降低了ROS的含量并抑制了NF-κB途径的激活。结论高葡萄糖可降低N-CDH表达并促进NP细胞衰老。 N-CDH的过表达可以通过调节ROS /NF-κB通路来减弱高糖诱导的NP细胞衰老。这项研究表明N-CDH是减缓DM介导的椎间盘NP变性的潜在治疗靶标。

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