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Sinapic Acid Inhibits IL-1β-Induced Apoptosis and Catabolism in Nucleus Pulposus Cells and Ameliorates Intervertebral Disk Degeneration
Journal of Inflammation Research ( IF 4.5 ) Pub Date : 2020-11-10 , DOI: 10.2147/jir.s278556
Jin-Feng Huang 1, 2 , Xuan-Qi Zheng 1, 2 , Jia-Liang Lin 3 , Kai Zhang 4 , Hai-Jun Tian 4 , Wen-Xian Zhou 1, 2 , Hui Wang 1, 2 , Ze Gao 5 , Hai-Ming Jin 1, 2 , Ai-Min Wu 1, 2
Affiliation  

Background: Low back pain (LBP) is a very common condition and leads to serious pain, disability, and price tag all over the world. Intervertebral disk degeneration (IDD) is one of the major reasons that contributed to LBP. The levels of interleukin 1 beta (IL-1β) increase significantly in degenerative disks. IL-1β also accelerates IDD. Sinapic acid (SA) has the effect of anti‐inflammatory, antioxidant and antimicrobial. However, the effect of SA on IDD has never been studied. Therefore, the aim of this study was to figure out whether SA has protective effect on nucleus pulposus (NP) cells and further explore the possible underlying mechanism.
Methods: The nucleus pulposus (NP) tissues of rats were collected and cultured into NP cells. The NP cells were stimulated by IL-1β and treated with SA. In vitro treatment effects were evaluated by ELISA, Western blot assay, immunofluorescence, TUNEL method and real-time PCR. We conducted percutaneous needle puncture in the rat tail to build intervertebral disk degeneration model and treated rats with SA. In vivo treatment effects were evaluated by hematoxylin and eosin (HE) and safranin O (SO) staining and magnetic resonance imaging (MRI) method.
Results: Our results showed that SA not only inhibited apoptosis but also suppressed inflammatory mediators including nitric oxide (NO), prostaglandin E2 (PGE2), cyclooxygenase 2 (COX-2), inducible nitric oxide synthase (iNOS) interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α) in IL-1β-stimulated NP cells. As to extracellular matrix (ECM), SA could increase collagen II and aggrecan levels and reduce the expression of MMP13 and ADAMTS5 during the stimulation of IL-1β. Furthermore, SA could activate nuclear factor‐erythroid 2‐related factor‐2 (Nrf2) to inhibit nuclear factor κB (NF‐κB) induced by IL‐1β. Nrf2 knockdown partly reduced the protective effect of SA on NP cells. Correspondingly, SA ameliorated IDD by promoting Nrf2 expression. In vivo results also showed that SA could delay the progression of IDD.
Conclusion: In conclusion, we demonstrated that SA could protect the degeneration of NP cells and revealed the underlying mechanism of SA on Nrf2 activation in NP cells.



中文翻译:

芥子酸抑制 IL-1β 诱导的髓核细胞凋亡和分解代谢并改善椎间盘退变

背景:腰痛 (LBP) 是一种非常常见的疾病,会导致世界各地的严重疼痛、残疾和价格标签。椎间盘退变 (IDD) 是导致 LBP 的主要原因之一。白细胞介素 1 β (IL-1β) 的水平在退行性椎间盘中显着增加。IL-1β 也加速 IDD。芥子酸(SA)具有抗炎、抗氧化和抗菌作用。然而,从未研究过 SA 对 IDD 的影响。因此,本研究的目的是弄清楚SA是否对髓核(NP)细胞具有保护作用,并进一步探索可能的潜在机制。
方法:收集大鼠的髓核(NP)组织并培养成NP细胞。NP细胞由IL-1β刺激并用SA处理。通过ELISA、Western印迹法、免疫荧光法、TUNEL法和实时PCR评价体外治疗效果。我们在大鼠尾部进行了经皮针刺,以建立椎间盘退变模型并用SA处理大鼠。通过苏木精和伊红(HE)和番红O(SO)染色和磁共振成像(MRI)方法评估体内治疗效果。
结果:我们的研究结果表明,SA 不仅抑制细胞凋亡,而且抑制炎症介质,包括一氧化氮 (NO)、前列腺素 E2 (PGE2)、环氧合酶 2 (COX-2)、诱导型一氧化氮合酶 (iNOS) 白细胞介素 6 (IL-6) 和IL-1β刺激的NP细胞中的肿瘤坏死因子α(TNF-α)。对于细胞外基质 (ECM),SA 在 IL-1β 刺激过程中可增加胶原蛋白 II 和聚集蛋白聚糖的水平,并降低 MMP13 和 ADAMTS5 的表达。此外,SA 可以激活核因子-红细胞 2 相关因子-2 (Nrf2) 以抑制由 IL-1β 诱导的核因子 κB (NF-κB)。Nrf2 敲低部分降低了 SA 对 NP 细胞的保护作用。相应地,SA 通过促进 Nrf2 表达来改善 IDD。体内结果还表明,SA 可以延缓 IDD 的进展。
结论:总之,我们证明了 SA 可以保护 NP 细胞的退化,并揭示了 SA 对 NP 细胞中 Nrf2 激活的潜在机制。

更新日期:2020-11-12
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